Emotional paralysis

Introduction "Emotional paralysis" is a phenomenon that exists in many patients with post-traumatic stress disorder. Post-traumatic stress disorder (PTSD), also known as delayed psychogenic reaction, is a delayed response caused by a stressful event or situation. PTSD is a delayed and/or persistent response to unusually threatening, catastrophic events. Traumatic events are necessary for the diagnosis of PTSD, but not sufficient conditions for PTSD to occur. Although most people experience varying degrees of symptoms after traumatic events, studies have shown that only some people eventually become PTSD patients.

Cause

(1) Causes of the disease

PTSD is caused by stressful events or situations, including natural disasters and man-made disasters such as wars, serious accidents, witnessing the tragic death of others, being tortured, victims of terrorist activities, and being raped. If there are predisposing factors, personality disorder or history of neurosis, it can reduce the defense against stressors or aggravate the disease process.

(two) pathogenesis

So far, the pathogenesis of this disease has not yet been elucidated. It is now well established that traumatic events are necessary conditions for the onset of post-traumatic stress disorder, but they are not sufficient conditions for their occurrence. Although most people experience varying degrees of symptoms after traumatic events, only some people eventually become post-traumatic stress disorder, and many factors affect post-traumatic stress disorder, such as a family history of mental disorders. With past history, psychological trauma in childhood (such as suffering from sexual abuse, divorced parents before the age of 10), introverted and neuroticism, other negative life events before and after the traumatic event, poor family, poor physical health, etc. These phenomena are still in the in-depth study. The relevant information is as follows:

The study concluded that the clinical features of PTSD [can not recover from trauma for a long time; partial confusion of sensory impressions and reminiscence of messy fragments, manifested as repeated "flashbacks"; dissociation of symptoms and somatization] is due to central nervous system stress The memory process of information has obstacles, making the conditional fear reaction difficult to suppress or excessive inhibition. The current mechanisms for its generation include the following:

1. Memory system disorders in the brain: Neurophysiological and neuropsychological studies point to normal intracranial memory systems and their working patterns: there are at least two major memory-related systems in the brains of higher mammals: a system with The limbic system is the main link, which is related to cognitive memory. The other system is based on the basal ganglia, which is related to the acquisition of habits and the memory of adaptive response. The former is the neural circuit of declarative memory, and the latter is the non-declarative neural circuit. Both systems require input from the cerebral cortex to enter the operational state. The cerebral cortex sensory area, which is stimulated to activate, usually acts as a trigger for memory initiation. At least two pathways are formed from the primary sensory projection zone: one to the dorsal side It is connected to the motion system of the frontal lobe and the other to the ventral side, which is connected to the limbic system of the temporal lobe. The neural circuit of declarative memory is that the visual signal reaches the visual cortex from the retina through the outer geniculate body, and the visual signal of the cortex needs to be processed by multi-level neurons to be recognized. In addition to the primary cortex V1, the integration of advanced visual cortex such as V2, V3 and V4, and the temporal lobe are required to complete the identification of more complex visual signals. It then connects back to the edge system and enters the recall loop. The limbic system mainly includes the external olfactory and entorhinal cortex, the almond complex, the hippocampal formation and the side hippocampus. These medial temporal margin structures project directly onto the medial nucleus of the thalamus (including the giant cell part of the dorsal medial nucleus and anterior nuclei), and can also be indirectly projected to the medial nucleus of the thalamus via the bed nucleus and the papillary body of the final streak. The medial nucleus of the thalamus re-projects to the ventral medial portion of the frontal lobe, including the frontal cortex, medial prefrontal cortex, and cingulate cortex. These three parts of the limbic system, the medial temporal lobe, the medial thalamus, and the ventral medial frontal lobe are three key segments in the cognitive memory (ie, declarative memory) circuit.

The test results on the apes have proved that if one of the links is damaged, the animal cannot complete the task operation with cognitive memory. These three parts of the limbic system are the gateway to the basal forebrain cholinergic system, which is considered to be another brain structure important for cognitive memory. The cholinergic system has a two-way connection with the limbic system and can be projected into a wide area of the cerebral cortex, thus forming a neural circuit of declarative memory. In this memory loop, the thalamus is the gate that the outside world perceives information into the brain; the amygdala is part of the limbic system and is involved in the processing and recall of emotions. Here, the importance of the information will be assessed, and thus stimulate emotions and behaviors such as anxiety, escape, and resistance; the hippocampus is also part of the limbic system responsible for the ingestion and recall of information related to time and space. It can be considered as a database of the brain, its information is arranged in different categories, without emotional color, loading "substantial information." The frontal lobe is primarily responsible for the integration of multiple information and plans for future behavior. Because it also provides memories of past information, it is also a platform for planning the future.

WJJacobs and J.Metcalfe use the "Hot system/Cool system" to explain the memory working mode under stress and stress. The "cold integration system" refers to the recording and copying of the hippocampal memory system is objective, the program Spatial and temporal storage in the form of self-biography; its integration is a complete, neutral, informative, easy-to-control program, and is holistic. In contrast, the heat integration system means that the amygdala is direct, fast, very emotional and irreversible, fragmented; its memory is stimulated and is a sign of renewedness, like a simple response. (De Kloet et al, 1993) Studies indicate that the thermal/cold system is different for increasing stress response: at low levels of stress response, mineralocorticoid receptor production in the hippocampus increases adaptive stress Reaction, but at high levels of stress response, the continuous binding of the glucocorticoid receptor to the mineralocorticoid receptor causes the hippocampus to become unresponsive, even becoming dysfunctional in higher stress responses; The thermal system exhibits a simple increase in response to increasing stress response. Therefore, at the level of traumatic stress, the cold system becomes dysfunctional and the thermal system becomes highly reactive at this time, which means that the intrinsic coding becomes fragmented under such conditions, rather than spatial time integration, enrichment and integrity. Coherent.

2. Imprints of memory and synaptic plasticity (LTP) studies of the central nervous system have shown that normal memory impression formation and learning are associated with long-term synaptic enhancement (LTP). In the afferent fibers of the hippocampus and the inner loop of the hippocampus, three excitatory synaptic connections are formed: CA4 granulosa cells from the anterior perforant path (PP) hippocampal dentate gyrus; Mossy fiberCA3 pyramidal cells; Schaffer collaterals from CA3 pyramidal cellsCA1 pyramidal cells. The study found that evoked potentials classified by stimulation intensity were recorded near CA4, CA1 and CA3 neurons to form LTP. The two main factors inducing LTP are the frequency and intensity of tonic stimulation. A certain intensity of stimulation can increase the amplitude of EPSP caused by a single stimulus, while a certain frequency of stimulation can cause a superposition effect on EPSP, the result of which makes the postsynaptic membrane Depolarization reaches a certain level, so that the Mg2 in the NMDA receptor channel prevents Ca2 influx, so that when the transmitter binds to the NMDA receptor, the channel opens, the Ca2 inflow, the intracellular Ca2 concentration increases, and then Triggering a series of biochemical reactions that alter the properties of the membrane, leading to LTP production. Ca2 plays an important role in the LTP induction process, and LTP effect can not be induced in low Ca2 solution. High concentration of Ca2 can directly induce LTP and enhance the induction effect. However, excessive Ca2 concentration may cause damage to the hippocampus. Animal experiments in molecular biology showed that the hippocampal cells were overloaded within 72 hours after the electrical stimulation of the experimental animals in the subthreshold stimulation group. The continuous increase of intracellular free Ca2 concentration can promote the deposition of a large amount of Ca2 in the mitochondria, leading to the oxidative phosphorylation of the electron transport chain, the ATP synthesis disorder, resulting in abnormal ion concentration in the nerve cells and seriously affecting the excitability of neurons; Continuous increase in intracellular free Ca2 concentration can also trigger a variety of neurotoxic effects by binding to Ca2 binding proteins, as well as post-synaptic excitatory conduction, Ca2 influx-induced synaptic activity changes, and activity-dependent nuclear gene long-term events. There is an important significance in the regulation of expression.

Therefore, when intracellular Ca2 overload leads to abnormal regulation of CaM-CaMKIIa signaling pathway, it can trigger these complex signal transduction chains in nerve cells and initiate multi-level nuclear transcription factors, especially the gene regulatory pathways mediated by dependent response elements. It induces long-term gene expression and regulation abnormality of nerve cells, which promotes the change of CNS neural plasticity, and ultimately leads to abnormal cognitive and dysfunctions such as learning, memory and behavior. However, under strong stress, the patient may cause Ca2 overload in the hippocampus, which may cause long-term effects or synaptic morphological changes that are difficult to regress under stress, leading to traumatic memory disorders.

3. Neuroendocrine dysfunction: The hypothalamic-pituitary-adrental (HPA) axis system plays an important role in the regulation of stress response. Corticotropin-releasing factor (CRF) is one of the most important neuromodulators that regulate endocrine, autocrine and behavioral responses induced by stress in mammals. Bremner et al. found that the CRF content in cerebrospinal fluid of patients and normal controls was significantly higher than that of the latter, suggesting that there is a neuroendocrine regulatory disorder in HPA axis in patients with PTSD. Yehuda (1998) found that PTSD differs from other stressed individuals in the following ways:

1 Low levels of cortisol (the level of cortisone in patients with PTSD is significantly reduced in urine and saliva).

2 increased sensitivity of the glucocorticoid receptor.

3 strong negative feedback suppression.

4 The systems of the hypothalamic-pituitary axis become more and more sensitive. In addition, Yehuda (2003) found that the cortisone levels of PTSD patients and their offspring were on average.

The glucocorticoid system also plays an important role in the regulation of HPA axis, and cortisol may have a significant anti-stress effect. Yehuda and other studies have shown that urinary mean cortisol levels in patients with PTSD are significantly reduced, plasma basal cortisol levels are reduced, and the number of glucocorticoid receptors in lymphocytes is increased. Dexamethasone inhibition experiments show that patients with HPA axis negative feedback inhibition are enhanced, speculative After acute traumatic stress or chronic stress, sustained low cortisol response and HPA axis negative feedback inhibition were enhanced. Low levels of cortisol can prolong central and peripheral NE utilization, which in turn may affect the consolidation of memory in events. Because animal studies have shown that sympathetic activity promotes learning ability based on low cortisol levels; if this process occurs in PTSD patients, the memory of traumatic events is consolidated and accompanied by a strong sense of subjective pain; Pain can change a person's mental activity (perception, thinking, especially the risk-related sensation and ability to deal with threats), making recovery slower and more responsive, possibly by affecting the body's ability to integrate traumatic experiences, ultimately leading to PTSD.

In the overall stress neuroendocrine response, adrenal glucocorticoids are an objective indicator of changes in cognitive status, and glucocorticoid levels are significantly elevated under acute stress and chronic stress. The hippocampus concentrates a higher concentration of adrenal glucocorticoid receptors than the other brain regions, namely the class I mineralocorticoid receptor (MR) and the class II glucocorticoid receptor (MR), and is therefore particularly sensitive to stress processes. A brain area. When the adrenal glucocorticoid receptor binds to most adrenal glucocorticoids, the class II glucocorticoid receptor binds very rarely. When the body is under stress, the circulating concentration of adrenal glucocorticoids increases, and the binding of class II glucocorticoid receptors is strengthened. Electrophysiological studies have found that class I mineralocorticoid receptors can increase hippocampal neuroplasticity by increasing long-term potentiation (LTP). The class II glucocorticoid receptor has the opposite effect on LTP.

Therefore, long-term stress-induced release of adrenal glucocorticoids, or long-term treatment with adrenal glucocorticoids, can lead to a decrease in hippocampal capacity, dendritic atrophy in the hippocampal CA3 region, changes in the synaptic structure, and a large number of pyramidal cells. Thinning and shedding, it was also found that the occurrence of dentate gyrus cells was inhibited. In general, there is an inverted U-type relationship between the amount of cognitive dysfunction in the hippocampus and the acute effects of adrenal glucocorticoids. Chronic stress causes a persistent increase in glucocorticoids, causing abnormal expression of hippocampal genes, leading to learning and memory. Damaged.

4. Neuroanatomical changes and susceptibility of PTSD: PET studies have shown severe cerebral blood flow in some areas of PTSD, including the frontal cortex, anterior cingulate gyrus, and prefrontal cortex (Brodmann's areas 2, 9), The fusiform gyrus/temporal lobe cortex, and in the posterior cingulate gyrus, the activation of the left subcortical related area and the motor cortex increased, these areas are related to the memory loop. PET and functional nuclear magnetic MRI confirmed that the amygdala and anterior marginal zone were more responsive to traumatic stimuli; the anterior cingulate gyrus and the preoptic area were less reactive (these areas were associated with fear responses). LeDoux (1998) found that the fear response of the body is related to the amygdala, which combines the acquired sensory information into the adaptive response (wrestling or escape) to prepare the body for action (such as cardiac output from the gastrointestinal tract). Turning to muscle, stress hormones flow into the bloodstream to provide energy). These activities occur prior to the "thinking" part of the brain (involving the hippocampus in the cerebral cortex) to estimate the threat, indicating that the amygdala acts as a "hijacked" here. Therefore, LeDoux (1998) proposes that the amygdala is the expression of the body, the stated part, which activates the fear response for any distant problem that matches the wound without the need to detect and make decisions through the cerebral cortex. The hippocampus is responsible for long-term statement of memory and filing new memories. The hippocampus is associated with the amygdala, so it can be controlled. But there are two issues to note:

1 From the amygdala to the hippocampus is a rapid channel, and the other channel that is returned suggests that the uniform of the hippocampus on the amygdala is not always possible; also the reduction of the median frontal cortex (a structure that inhibits the function of the amygdala), Strengthening the expression of the amygdala increases the concentration and frequency of traumatic memory. The hippocampal volume reduction in PTSD patients (Yehuda) can explain the patient's lack of declarative memory. But I wonder if this happened before the trauma, but it is the susceptibility factor of PTSD.

2 (Linda Carroll, 2003.7) found that the Anterior Cingulate Cortex (ACC) of patients with PTSD was significantly smaller than the normal population. ACC played a role in helping the patient to notice the self or the environment during the emotional modulation of the brain, while PTSD The patient's ACC function is impaired, but it does not indicate that the PTSD is less pre-traumatic ACC, but once it occurs as a PTSD, the ACC portion is invaded, which helps us understand the clinical symptoms of patients with PTSD. In addition, EEG studies also showed that patients with PTSD had decreased waves and increased waves. The excitability increased beyond the medial cortex plane and left occipital region of the frontal lobe. The II excitability increased in the frontal lobe, and the wave range exceeded the frontal area. Excessive excitability of the cortex, prolonged wakefulness, imbalance of activation of the frontal lobe, and increased wave excitation can help explain hippocampal volume changes, indicating neurobiological changes in PTSD patients.

Additional studies have shown that early severe stress responses and inadequate treatment can produce a cascade of neurobiological changes that potentially affect sustained brain development. These changes are manifested at multiple levels, the structure and function of the neurohormone [Hypothalamus-pituitary-adrental (HPA) axis system]; the central part of the white matter and the plastid and the left neonatal cerebral cortex, hippocampus and The development of the amygdala becomes sparse, reducing the electrical irritability of the frontal branches and the excitability of the cerebellum. Due to the sparseness of the forehead and the sparseness of the anterior cingulate gyrus, it eventually extends to the dysfunction of the amygdala. At a certain stimulation threshold, the frontal lobe cannot perform higher-level regulation of the lower level, resulting in the right almond. Activation of the body. Lack of inhibition of the first activated neurological level, maintaining a high response (negative symptoms), reduces the flexibility and more automatic regulation (positive symptoms).

In addition, the sputum return, the anterior cingulate gyrus and the amygdala system are also associated with the autonomic nervous system. The disorder of the above system also leads to the dysfunction of the autonomic nervous system, which will show a pair of non-associated things over a long period of time. The automatic control mode, which combines the sympathetic and parasympathetic components, or the automatic control mode of unpaired non-related things, both represents the separation of the autonomic nervous system: part of the change is missing. That is to say, the autonomic nervous system is too easy to be replaced by an auto-balancing state. Once replaced, it is difficult to establish a balance, which is incapable of regulating the retraction and recovery of the vagus nerve from psychological stress. Neurobiology changes due to early damage make these individuals more susceptible to PTSD in adulthood.

Current research has shown that early trauma can cause neurobiological changes in individuals to become susceptible to PTSD; it also explores that excessive or persistent mental stress leads to impairment of the memory loop and regulation of central excitatory and inhibitory processes. The expression of neurotransmitters in the changes changes, leading to the formation of PTSD. However, the brain map of the entire intact pathological mechanism is not fully understood, but the discussion of the generation process of memory impressions along the mental stress, especially its neurobiology and neuropathophysiology, may finally reveal its mechanism.

an examination

Related inspection

Brain CT examination

PTSD is characterized by a series of characteristic symptoms following a major traumatic event.

1. Repeatedly reproduce the traumatic experience: patients re-experience traumatic events in various forms, intrusive memories, repeated repetitive traumatic dreams, painful dreams, vivid experiences of recurrence of stressful events Repeated traumatic dreams or nightmares, repeated recurrence of traumatic experience; sometimes patients have a state of separation of consciousness, duration can vary from a few seconds to a few days, called Flash back. At this time, the patient seems to be completely in the situation when the traumatic event occurs, and re-expresses the various emotions accompanying the event. When a patient faces, contacts, or resembles an incident, situation, or other cues associated with a traumatic event, there is often a strong psychological distress and physiological response, such as the anniversary of the event, similar weather, and various similar scenarios. The psychological and physiological response of the patient. (Davidson JRT, 1995; American Psychiatric Association, 1994).

2. Persistent avoidance: There is a constant avoidance of trauma-related stimuli in patients after a traumatic event. The objects to be avoided include specific scenes and situations, related thoughts, feelings and topics. Patients are reluctant to mention relevant events and avoid related conversations. Media interviews after traumatic events and forensic procedures involving legal procedures often bring to the parties. It is a great pain. Losing memory for certain important aspects of traumatic events is also seen as one of the manifestations of avoidance.

While avoiding, there is also the expression of mental numbness or emotional paralysis. The patient gives a feeling of indifference to the whole, consciously has no interest in anything, and is equally interested in activities that have been keen on the past, and feels alienated from the outside world. Even out of contact with others; no contact with others; no reaction to the surrounding environment; lack of pleasure; avoiding memories of past traumatic activities, fear and avoiding the feeling of suffering trauma is also more common. It seems that there is no indulgence in everything. It is difficult to express and feel the emotions of all kinds of exquisite hopes. I am disheartened by the future, and I am resigned to my heart. When I am serious, I am so mad that I have negative thoughts and suicide attempts.

3. Increased levels of persistent anxiety and alertness: manifested as a spontaneously high alert state, such as difficulty falling asleep, not restful, vulnerable to fright, do not concentrate on doing things, etc., and often have autonomic symptoms such as palpitation, shortness of breath and so on.

China's three widely used CCMD, ICD and DSM diagnostic systems have diagnostic criteria for PTSD. The definition and diagnosis of this disorder are basically the same. However, relatively speaking, DSM-IV defines PTSD more comprehensively and specifically, so the diagnostic criteria of DSM-IV are mainly introduced here (American Psychiatric Association, 1994; Stein MB, 1997). DSM-IV diagnostic criteria for PTSD include 6 major items from A to F, A is the event standard, B, C, and D are symptom criteria, E is the disease standard, and F is the severity standard.

Differential diagnosis

1. Acute stress disorder and adaptation disorder

Some patients have obvious mental symptoms and strong mental pain after major traumatic events, but they do not fully meet the diagnostic criteria for post-traumatic stress disorder. Some patients are consistent with post-traumatic symptoms in terms of symptoms, duration and severity. The corresponding criteria for stress disorder, but the induced events are general stress events such as loss of love, dismissal, and so on. Both of the above conditions should not be diagnosed as post-traumatic stress disorder, but should be considered as an adaptation disorder. The main difference between acute stress disorder and post-traumatic stress disorder is the onset time and course of disease. The onset of acute stress disorder is changed to 4 weeks after the event, and the course of disease is shorter than 4 weeks. When the symptoms persist for more than 4 weeks, the diagnosis should be changed to post-traumatic stress disorder.

2. Other mental disorders

(1) Depression: This disease has the interest to decline, alienation from others, feeling the future, and there are also sad experiences, similar memories of "touching the scene", emotional changes, etc., but there are still differences between the two. However, simple depression disorders do not have intrusive memories and dreams associated with traumatic events, nor do they evade specific topics or scenarios. The depression mood of depression involves a wide range of aspects, including usual interests, daily preferences, and personal future. Negative, inferiority or suicide attempts are also common.

(2) Anxiety neurosis: In the case of delayed psychogenic response with persistent alertness and autonomic nervous system symptoms, it should be differentiated from chronic anxiety. Anxiety disorders often have excessive anxiety about their own health, more complaints about the body, and even a tendency to suspect, but no obvious factors of mental trauma.

(3) Obsessive-compulsive disorder: It can express recurrent obsessive-compulsive thinking, but it often shows inappropriateness and there is no unusual life event before the disease, so it is different from post-traumatic stress disorder.

(4) Severe mental disorders: schizophrenia and mental disorders associated with physical illness can have hallucinations and illusions, but these diseases do not have an unusual traumatic experience before the disease, and the symptoms are different, so It is not difficult to distinguish from the hallucinations and illusions of post-traumatic stress disorder.

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