Midbrain Activation For Adults Pdf Free
Objective To investigate the activation of the amygdala, midbrain, and ventral striatum during an aversive pavlovian conditioning task in patients with schizophrenia and healthy control participants using functional magnetic resonance imaging.
Midbrain Activation For Adults Pdf Free
Results Patients with schizophrenia showed abnormal activation of the amygdala, midbrain, and ventral striatum during conditioning. Activation of the midbrain in response to neutral rather than aversive cues during conditioning was correlated with the severity of delusional symptoms in the patient group (corrected P = .04).
Conclusion Inappropriate activation of the midbrain in response to neutral stimuli during conditioning is associated with the severity of delusional symptoms in patients with schizophrenia.
Region of activation in midbrain, which correlated significantly with childhood physical abuse, as assessed by the CTQ, in those with borderline personality disorder. Red areas show activation meeting threshold P
Previous studies have identified a relationship between childhood trauma and altered emotion regulation, as well as behavioural responses to emotional stimuli in BPD.12, 32 Childhood adversity has also been strongly associated with the development of symptoms of the disorder, and more generally with the development of psychotic symptoms across a range of disorders.5, 6, 15 We investigated the relationship between childhood adversity and brain responses to emotional stimuli in participants with BPD. Using this analysis, we identified a significant association between brain activation in a network of regions including the midbrain, medial frontal gyrus, pulvinar and cerebellum, and previous experience of physical abuse as measured by the CTQ.
The midbrain is the key site of dopaminergic afferents to the limbic system and is known to be involved in emotion processing.33 Dysfunction of this brain region is widely theorised to contribute to the development of psychotic symptoms in schizophrenia.17, 34 The present results suggest that, in patients with BPD, childhood physical abuse results in an increased response of the midbrain to negative (fearful) emotional stimuli. We also found that individuals with BPD who experienced childhood physical abuse may be particularly vulnerable to the development of psychotic symptoms, via midbrain dysfunction, when exposed to negative emotional stimuli in adulthood. These findings provide a potential biological rationale for the use of antipsychotic medications to ameliorate psychotic symptoms in BPD.35 However, fMRI is only an indirect measure of dopamine system activation and the results would be strengthened by future studies using more direct measures such as positron emission tomography. Furthermore, the psychotic symptoms reported by BPD sufferers were generally at the milder end of the range of severity as assessed by the PANSS, and it may be these symptoms such as suspiciousness and paranoid ideation, to which BPD sufferers are particularly vulnerable.
The present study demonstrates a significant association between childhood trauma and brain activation in BPD, and suggests a link between childhood physical abuse and psychotic symptoms in adulthood, which may be mediated through altered midbrain activation. To the authors' knowledge, this is the first time such correlations have been identified in a BPD population. These results may help explain the sensitivity of many individuals with the disorder to negative emotional stimuli, and, in particular, the tendency of sufferers to develop psychotic symptoms at times of emotional stress. Altered midbrain activation may also underlie the response to antipsychotic treatment seen in patients with BPD. The results also support the use of early psychological interventions in individuals with this diagnosis to ameliorate negative responses to environmental stimuli, and highlight the importance of managing emotional stressors in sufferers. They illustrate the key role of early-life experience in modulating midbrain activation, which may be of relevance to a range of psychiatric disorders, particularly those in which psychotic symptoms are a significant feature.
There are some limitations to the study, which should be acknowledged. First, the majority of participants in the BPD group were taking medication at the time of the study. It is possible, though unlikely, that medication effects may have contributed to the group difference in activation noted in the cuneus and in the correlations noted between brain activation and childhood trauma. However, the likelihood of this is very low, given the variation of medication use across participants and the specific effects of childhood abuse seen in the within-group correlation analyses. Second, the BPD participants in the current study were predominantly female consistent with clinical populations in the UK but not with epidemiological studies, which point to a more balanced sex ratio.3 Participants in the current study also had a relatively broad age range, but this was closely balanced across groups. Third, the participants in the current study were of higher-than-average IQ, potentially representing the local demographics and a tendency for more able individuals to take part. Fourth, the findings within the midbrain were within an a priori area of interest, although these findings were strengthened by the subsequent specific association of activation in this region with severity of psychotic symptoms. Fifth, there was insufficient range of CTQ scores in the control population to determine whether the relationship between physical abuse and midbrain activation is also seen in individuals without BPD, which would require larger samples. Sixth, although the current research has identified a trend towards midbrain activation mediating the relationship between childhood physical abuse and psychotic symptoms in adulthood in BPD, this finding fell just short of formal statistical significance. Further investigation is required, ideally using larger sample sizes, to better determine the role of the midbrain in the development of psychotic symptoms. Similarly, this relationship in other psychiatric disorders should be investigated to elucidate whether this effect is specific to BPD.
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The mesolimbic dopamine system is the major neuromodulatory system implicated in motivated learning of valuable information17. It has been proposed that the motivation to learn engages mesolimbic dopaminergic circuits to support plasticity in the hippocampus18,19. Consistent with this account, fMRI studies in humans have shown that the motivation to learn, inspired by both intrinsic and extrinsic rewards, is accompanied by increased anticipatory activation in the dopaminergic midbrain18. Such increases in midbrain BOLD have been shown to correlate with PET measures of dopamine release in target regions20. During anticipatory midbrain activation, greater functional connectivity between the midbrain and regions in the medial temporal lobe, including the hippocampus (HPC)18,19,21, predicts memory. Intriguingly, in one such study where participants were motivated by intrinsic curiosity, memory was enhanced not only for the information of interest, but also for temporally proximal irrelevant information19, suggesting a sustained state of enhanced encoding.
Independent lines of work suggest that the hippocampus can express different functional states that reflect neuromodulation, and that these may manifest as physiological signatures associated with distinct patterns of activity in the hippocampus. First, the hippocampus receives inputs from the dopaminergic midbrain, including ventral tegmental area (VTA)22,23,24, and midbrain projections modulate hippocampal physiology and influence performance on memory tasks25,26,27,28,29. Studies of place cells in rodents have also shown that place field stability is influenced by task goals, dependent on midbrain modulation1,30. Such shifts in response properties and circuit function have physiological signatures that could manifest in BOLD activation patterns31. Indeed, in humans, dopamine receptor density has been associated with variability in the BOLD signal intensity in the hippocampus32. The anatomical separation of mesolimbic terminals relative to dopamine receptors in the hippocampus is ill-suited to temporally precise signals17 and further suggests that midbrain dopamine regulates expression of sustained functional states in the hippocampus conducive to encoding1,17,30,33.
Here, we were motivated by the premise that hippocampal multivoxel activation patterns may manifest, in addition to representations of information, neural states conducive to memory formation. We reasoned that if conducive state-spaces exist, their instantiation would be a candidate mechanism for memory enhancement by neuromodulation. To isolate patterns associated with neuromodulatory effects from those representing information to be encoded, we examined intervals prior to the presentation of memoranda. We hypothesized that while awaiting valuable information, (i) hippocampal states would reflect the univariate activation of dopaminergic midbrain VTA, (ii) that instantiation of patterns associated with memory-conducive neural states would predict subsequent memory, and (iii) that memory-conducive states would account for previously reported associations between increased midbrain VTA activation and memory formation.