驾驶人员路怒情绪与驾驶风格及攻击行为相关分析

目的 了解驾驶人员的路怒情绪与驾驶风格及攻击性驾驶行为之间的相关性。方法 2015年6-8月,采用方便抽样法抽取河北省沧州、唐山等市313名驾驶人员,使用多维度驾驶风格量表、驾驶人愤怒表达量表及驾驶风格量表进行调查。结果 在驾驶风格因子中的冒险型、愤怒型和焦虑型方面,女性驾驶人员得分分别为（18.89±6.08）、（14.27±4.58）和（30.01±9.78）分,均低于男性驾驶员的（20.57±4.94）、（16.88±4.66）、（32.78±7.23）分,差异均有统计学意义（P<0.01）;<2年驾龄的驾驶人员攻击行为的驾驶空间占用、获得领先和人际攻击维度的得分高于驾龄>5年的驾驶人员;2～5年驾龄的驾驶人员攻击行为的无视他人和驾驶空间占用、获得领先、人际攻击维度的得分均高于驾龄>5年的驾驶人员（P<0.05）;职业与非职业驾驶人员在愤怒情绪的操作强度、操作频率、言语攻击、对车发泄、自我调节维度得分差异均有统计学意义（均P<0.01）;私家小汽车驾驶人员在愤怒情绪的操作强度、操作频率、言语攻击和对车发泄因子上的得分显著低于其他车型驾驶人员的得分（均P<0.01）;驾驶风格的冒险型和焦虑型因子与驾驶愤怒情绪各因子（P<0.01）及攻击性驾驶行为各因子（P<0.05）呈显著正相关;驾驶风格的愤怒型因子与驾驶愤怒情绪的操作强度、操作频率、言语攻击和自我调节呈显著正相关（P<0.01）,同时和攻击行为的无视他人、驾驶空间占用、快速前进和获得领先因子呈正相关（P<0.05）;焦虑型驾驶风格对攻击性驾驶行为有预测作用（β=1.830,P<0.001）。结论 驾驶人员的愤怒情绪与驾驶风格受性别、驾龄、驾驶车型及是否为职业驾驶员等因素的影响;驾驶人员在驾驶风格量表中得分越高,驾驶人员的愤怒情绪表现越强烈,在驾驶中越易出现攻击性驾驶行为。     

Devaluation,Loss, and Rage: A Postscript to Urban African American Youth with Substance Abuse

This article explores and discusses the sociocultural dynamics underpinning urban African American youths' use and misuse of substances and its connection to the invisible wounds of race-related trauma. A racially-sensitive framework is discussed as an intervention approach designed to address the special needs of urban Africa American adolescents maligned by, and suffering from, the complex interplay of substance misuse and rage.     

Serotonin 5-HT1A and 5-HT2/1C receptors in the midbrain periaqueductal gray differentially modulate defensive rage behavior elicited from the medial hypothalamus of the cat

Recent studies have established that the expression of defensive rage behavior in the cat is mediated over a descending pathway from the medial hypothalamus to the dorsolateral quadrant of the midbrain periaqueductal gray matter (PAG). The present study was designed to determine the roles played by 5-HT_1A and 5-HT_2/1C receptors in this region of PAG in modulating defensive rage behavior elicited from the cat's medial hypothalamus. Monopolar stimulating electrodes were implanted into the medial hypothalamus from which defensive rage behavior could be elicited by electrical stimulation. During the course of the study, the `hissing' component of the defensive rage response was used as a measure of defensive rage behavior. Cannula-electrodes were implanted into sites within the PAG from which defensive rage could also be elicited by electrical stimulation in order that 5-HT compounds could be microinjected into behaviorally identifiable regions of the PAG at a later time. Microinjections of the selective 5-HT_1A agonist, (+)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OHDPAT) (50 pmol, 2.0 and 3.0 nmol), into the PAG suppressed the hissing response in a dose-dependent manner. Administration of the selective 5-HT_1A antagonist, 4-iodo-N-[2-[4-(methoxyphenyl)-1-piperazinyl] ethyl]-N-2-pyridinyl-benzamide hydrochloride (p-MPPI) (1.5 and 3.0 nmol), blocked the suppressive effects of 8-OHDPAT upon hissing. In contrast, microinjections of the 5-HT_2/1C receptor agonist (+)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride ((+)-DOI hydrochloride) (0.01, 1.0 and 1.5 nmol) facilitated the occurrence of hissing elicited from the medial hypothalamus in a dose-dependent manner. Immunohistochemical analysis revealed the presence of 5-HT axons and preterminals throughout the PAG, and in particular, in its dorsolateral aspect which receives major inputs from the medial hypothalamus in association with defensive rage behavior. The overall findings of the study provide evidence that activation of 5-HT_1A and 5-HT_2/1C receptors within the midbrain PAG differentially modulate the expression of defensive rage behavior elicited from the medial hypothalamus of the cat.     

Evidence that substance P is utilized in medial amygdaloid facilitation of defensive rage behavior in the cat

The present study was designed to test the hypothesis that a major excitatory mechanism for the expression of feline defensive rage behavior involves the medial nucleus of the amygdala which utilizes substance P as a neurotransmitter in a direct output pathway that supplies the medial hypothalamus. In phase I of the experiment, stimulating electrodes were implanted into the medial amygdala and cannula electrodes were implanted into the medial and lateral hypothalamus from which defensive rage and predatory attack behavior could be elecited by electrical stimulation, respectively. Response latencies for defensive rage were significantly lowered after dual stimulation of the medial amygdala and medial hypothalamus relative to single stimulation of the medial hypothalamus alone. In phase II, dose- and time-dependent decreases in medial amygdaloid-induced facilitation of defensive rage were observed after the i.p. administration of the NK₁ antagonist, CP-96,345 (0.05, 2 and 4 mg/kg). In phase III of the study, the effects of microinjections of CP-96,345 placed directly into defensive rage sites within the medial hypothalamus (0.05, 0.5 and 2.5 nmol) upon medial amygdaloid modulation of this response were assessed. Again, intracerebral administration of this antagonist blocked the facilitatory effects of medial amygdaloid-induced facilitation of defensive rage in a manner parallel to that observed with peripheral administration of the NK₁ antagonist. The results suggest that the medial amygdala facilitates defensive rage by acting through a substance P mechanism at the level of the medial hypothalamus. Other experiments revealed that peripheral administration of the NK₁ antagonist: (1) had little effect upon the latency or threshold for elicitation of defensive rage, suggesting that the medial amygdaloid-substance P facilitatory mechanism acts in a phasic rather than tonic manner; and (2) also blocks the suppressive effects of medial amygdaloid stimulation upon predatory attack behavior elicited from the lateral hypothalamus. The latter finding suggests that similar neurochemical mechanisms regulate medial amygdaloid modulation of both forms of hypothalamically elicited aggression. The final aspect of this study utilized the combination of retrograde-tracing of amygdaloid neurons into the medial hypothalamus after microinjections of Fluoro-Gold into defensive rage sites, and the immunocytochemical analysis of substance P neurons within the amygdala. The data indicated that large numbers of retrogradely and immunocytochemically positive labeled cells were identified in the medial nucleus, including many that were double-labeled. The overall findings of this study support the hypothesis that the medial amygdala provides a powerful excitatory monosynaptic input to the medial hypothalamus for the expression of defensive rage behavior and that this mechanism is mediated, at least in part, via a substance P mechanism.     

Preoperative location of microcalcifications after macrobiopsy: failure of lipiodol

Accurate mark of macrobiopsy site, carried out borderline or malignant lesions, is very important for surgeons. We report a woman case, 68 year's old, who presents intraductal carcinoma diagnoses on macrobiopsy. On postbiopsy X-ray, we can note lipiodol used instead of clip to reaper macrobiopsy site. Our observation shows how lipiodol use is not adapted into this indication.     

Tic disorders in childhood

Despite our familiarity with tic disorders, their management remains challenging. The difficulty seldom relates to the diagnosis, which is usually based on the history, but rather in dealing with the impact of the tics and multiple comorbidities. The child and family must be educated and must be taught how to facilitate a positive attitude among others who come in contact with the patient. Knowledge and acceptance of the tics by other family members, peers, teachers, and coaches often become central to the child's well-being. Although many children can be managed without pharmacotherapy, medications are often central to achieving success. The goals of therapy and the appropriate choice of medication must be individualized. We are frequently challenged not only by the wide array of medication choices available but also by the decision of which symptom to treat first. The tics, despite being flamboyant, are often viewed by the child and family as less disabling than co-occurring conditions, such as attention-deficit hyperactivity disorder, obsessive-compulsiveness, or rage. Even when tics are the major issue, patients must define their goals for therapy. It is unreasonable to expect a complete resolution of tics and safety usually rules in favor of better tolerated but potentially less efficacious therapies. Developing strategies to minimize the lifelong impact of the multiple components of Tourette syndrome is an essential aspect of the care of these patients.     

Terror breeds terrorists

Abstract

Terrorism can be carried out by the state or by its citizens. The latter may be labelled ‘freedom fighters’ or ‘terrorists’ depending on the political context. One of the most important aetiological factors driving Islamic terrorists is the experience of alienation and shame. This sense of being made to feel totally invalidated, of feeling worthless in the eyes of the other, is at the root of rage and violent revenge, implying that the way the current ‘War on Terror’ is being fought by the United States and the United Kingdom can only lead to more terrorism and danger for our society.     

GABA receptor mediated suppression of defensive rage behavior elicited from the medial hypothalamus of the cat: role of the lateral hypothalamus

Recently, our laboratory has demonstrated that predatory attack behavior in the cat, elicited by electrical stimulation of the lateral hypothalamus, is suppressed following activation of the region of the medial hypothalamus from which defensive rage behavior is elicited [Han, Y., Shaikh, M.B., Siegel, A., Medial amygdaloid suppression of predatory attack behavior in the cat: II. Role of a GABAergic pathway from the medial to the lateral hypothalamus, Brain Res., 716 (1996) 72–83.]. The mechanism for this suppression is a direct GABAergic projection from the medial to lateral hypothalamus. The present study tested the hypothesis that the inhibitory relationship between these two regions of hypothalamus is reciprocal, namely, that a GABAergic neuron, which also projects from the lateral to medial hypothalamus, serves to suppress defensive rage elicited from the medial hypothalamus. Monopolar stimulating electrodes were implanted into lateral hypothalamic sites from which predatory attack behavior was elicited. In addition, cannula-electrodes were implanted into the medial hypothalamus for elicitation of defensive rage behavior and for microinjections of GABA compounds. Initially, in the absence of drug administration, the effects of dual stimulation of the lateral and medial hypothalamus upon response latencies were compared with those following single stimulation of the medial hypothalamus alone. Dual stimulation significantly (p<0.01) suppressed defensive rage behavior elicited from the medial hypothalamus. Then, administration of the GABA_A receptor antagonist, bicuculline (10–60 pmol), into medial hypothalamic sites from which defensive rage was elicited blocked the suppressive effects of lateral hypothalamic stimulation. The GABA_A receptor agonist, muscimol (0.3–30 pmol), microinjected into the medial hypothalamus, suppressed defensive rage elicited by single stimulation of the medial hypothalamus in a dose dependent manner. These suppressive effects of muscimol upon defensive rage were blocked following pretreatment with bicuculline (60 pmol). Administration of muscimol into adjoining regions of the lateral hypothalamus had no effect upon defensive rage, indicating its site specificity. Bicuculline (60 pmol) delivery into the medial hypothalamus had no effect upon defensive rage, suggesting the, presence of an episodic rather than tonic mechanism. A combination of immunocytochemical and retro grade tracing procedures were then employed to determine the origin of the putative GABAergic pathway projecting to the medial hypothalamus. In this experiment, the retrograde tracer, Fluoro-Gold (8%, 0.5 μl), was microinjected through a cannula-electrode in the medial hypothalamus from which defensive rage had been elicited. Following survival periods of 5–6 days, cats were perfused with 4% paraformaldehyde and brain tissue was processed for immunocytochemical staining of GABA neurons. Retrogradely labeled, immunopositively labeled, as well as Fluoro-Gold and GABA labeled cells, were identified in the lateral hypothalamus. Each type of neuron was distributed over wide regions of the lateral hypothalamus, extending from the area immediately caudal to the optic chiasm to the level of the posterior hypothalamus. Together, the behavioral pharmacological and anatomical data provide evidence of a direct inhibitory projection from the lateral to medial hypothalamus whose functions are mediated by GABA_A receptors. When coupled with our previous findings, these results reveal the presence of reciprocal GABAergic inhibitory pathways between the medial and lateral hypothalamus. The findings suggest that functions associated with either the lateral or medial hypothalamus, but not both, can be activated at a given time.     

Basal amygdaloid facilitation of midbrain periaqueductal gray elicited defensive rage behavior in the cat is mediated through NMDA receptors

The present study tested the hypotheses that: (1) defensive rage behavior eelicited from the midbrain periaqueductal gray (PAG) in the cat is facilitated from the basal complex of amygdala; and (2) such facilitation from this region of amygdala is mediated via a pathway in which excitatory amino acids acting upon NMDA receptors within the PAG are utilized as a neurotransmitter. In the first phase of this study, cannula electrodes were implanted into PAG sites for the elicitation of defensive rage behavior as well as for drug delivery. Then, a second monopolar electrode was implanted into the basal nucleus of amygdala from which facilitation of defensive rage could be obtained. As a esult of dual stimulation of the basal amygdala and PAG, response latencies for defensive rage were significantly lowered relative to PAG stimulation alone (P < 0.01). In the second phase of this experiment, 3 doses of a selective NMDA receptor antagonist, AP-7 (0.1, 0.5, 1.0 mg/kg), were peripherally (i.p.) administered in 5 animals. The results indicated a significant decrease in the facilitatory effects of amygdaloid stimulation in a dose and time dependent manner (P < 0.001). In the third phase, AP-7 was administered intracerebrally into PAG defensive rage sites in dose of 0.2 and 2.0 nmol. It was noted that intracerebral microinjections of AP-7 at the higher dose (2.0 nmol) also significantly suppressed the facilitatory effects of amygdaloid stimulation (P < 0.01); however, these effects were somewhat less potent then those observed following peripheral drug administration. A fourth phase of the study was conducted at the completion of the pharmacological experiments. Here, retrograde axonal tracing of amygdaloid neurons projecting to the PAG following Fluoro-Gold microinjections placed in defensive rage sites was coupled with an immunocytochemical analysis of the distribution of excitatory amino acid positive neurons present within the basal amygdala. The findings revealed the presence of high concentrations of glutamate and asparate positive cells located mainly within the basal and lateral nuclei of amygdala, while retrogradely labeled cells within the amygdala were confined to its basal complex, central nucleus and anterior amygdaloid area. More significantly, dense quantities of cells double labeled with both Fluoro-Gold and excitatory amino acids were identified within the basal complex of amygdala. Collectively, these findings support the view that neurons arising from the basal complex of amygdala serve to facilitate defensive rage behavior, in part, by virtue of their projections to the PAG and that this phenomenon is mediated by a mechanism utilizing excitatory amino acids that act through NMDA receptors.