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Attention-deficit/hyperactivity disorder and dementia – is there a link?
- C. Pinheiro Ramos, M. Magalhães, C. Baptista, R. Ribeiro, A. Gamito
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- Journal:
- European Psychiatry / Volume 66 / Issue S1 / March 2023
- Published online by Cambridge University Press:
- 19 July 2023, pp. S239-S240
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Introduction
Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by cognitive deficits and/or behavioral disturbances. The symptoms begin before 12 years and must cause an impact in different contexts. It is now recognized that in 40–60% of cases, ADHD symptoms persist into adulthood and old age, representing nearly 4% of adults and seniors.
Executive and memory deficits have been described in other neurodevelopmental disorders, such as autism, and older adults with these disorders are observed, later in life, with mild cognitive impairment (MCI) or dementia.
MCI is conceptualized as a prodromal stage of a neurodegenerative process, for which the pathological processes are not yet known. The term “MCI” is currently used to designate subjective complaints and performance below expected levels, in any cognitive domain.
There is, therefore, an overlap between ADHD and MCI in older adults, related to cognitive and behavioral symptoms. This overlap makes both syndromes difficult to distinguish, particularly in older patients.
ObjectivesTo highlight the importance of understanding the key processes of ADHD and MCI and how these entities may be related to each other.
MethodsNon-systematic review of the literature using Pubmed database. Papers were selected according to their relevance.
ResultsSleep disturbances are present in about 70% of adults with ADHD, and 59% of those with MCI. Depression and anxiety, respectively, are observed in about 44% and 35% of adults with ADHD, and 27% and 14% of those with MCI.
In the literature, the relationship between ADHD and MCI/Dementia remains unclear, although there are some hypotheses: (a) ADHD and MCI represent two points along a single pathophysiological continuum; (b) ADHD increases the risk for MCI and dementia (through an unrelated mediator); (c) ADHD and MCI manifest highly similar neurobehavioral symptoms through fundamentally distinct mechanisms (are unrelated). However, these three hypotheses are not mutually exclusive, i.e. ADHD may share common antecedent causal factors with MCI/Dementia and also increase the risk of MCI/Dementia through an unrelated mediator.
Neuroimaging evidence tends to support the hypothesis that neurobehavioral symptoms in ADHD and MCI manifest via distinct processes within the brain, with frontostriatal, frontal-temporo-parietal, and fronto-cerebellar abnormal networks in ADHD and progressive neurodegeneration in MCI.
ConclusionsWhether or not ADHD is a phase of a neurodegenerative process, the current criteria for the diagnosis of MCI or Dementia may not be appropriate or valid in individuals with a premorbid history of ADHD.
The criteria for the diagnosis of MCI/Dementia in adults with a previous diagnosis of ADHD should therefore be revised to rely more on functional outcomes.
Future neurobiological and epidemiological studies are needed, to explore the relationship between MCI/Dementia and ADHD, in older adults.
Disclosure of InterestNone Declared
EMOTIONAL PROCESSING IN ANOREXIA NERVOSA - WHAT IS THE ROLE OF NEUROMODULATION?
- C. Pinheiro Ramos, A. R. Vaz, A. Sampaio
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- Journal:
- European Psychiatry / Volume 66 / Issue S1 / March 2023
- Published online by Cambridge University Press:
- 19 July 2023, pp. S523-S524
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Introduction
Anorexia Nervosa (AN) is an Eating Disorder (ED), being globally characterized by a low body mass index (BMI), intense fear of gaining weight, and distorted body image that motivates extreme food restrictions. The consequence is massive weight loss.
AN is the third leading cause of chronic illness among adolescents and the leading cause of death among psychiatric conditions.
Among patients with AN it is common the occurrence of psychiatric comorbidities, particularly depressive and anxiety syndromes.
Negative emotions are very common and represent either primary aspects of the disease or arise secondarily to psychopathological or organic processes.
The therapeutic options for AN are scarce and only work for a small percentage of subjects.
It is known that difficulty in emotional regulation is one of the defining characteristics of ED, being a core feature of AN psychopathology.
ObjectivesTo highlight the importance of understanding the neurobiology of AN, how it is related to emotional processing and future directions for AN´s management.
MethodsNon-systematic review of the literature using Pubmed database. Papers were selected according to their relevance.
ResultsIn recent literature, in purging AN-type (neurobiology similar to Bulimia Nervosa - BN), binge eating is a method of emotional regulation, while in restricting AN-type, food restriction is the way to deal with emotions, mainly negative emotions.
It is known that in AN, patients tend to eat less than usual in response to a negative emotion and more than usual in response to a positive emotion. In BN, the neurobiology works in a mirrored way, patients eat less than usual in response to a positive emotion and more than usual in response to a negative emotion.
In short, in the face of negative emotions, subjects with AN respond with dietary restriction and, subjects with BN respond with binge eating. On the other hand, more positive emotions seem to resolve the maladaptive eating behaviours inherent to both ED, with AN and BN subjects tending towards more balanced eating behaviours.
One of the brain areas most implicated in the neurobiology of AN is the left dorsolateral prefrontal cortex (L-DLPFC), since this region is recognized as being involved in decision-making process and emotional regulation, and is therefore the target of novel and experimental treatment strategies, namely those related with neuromodulation, particularly Transcranial Magnetic Stimulation (TMS).
ConclusionsEmotional regulation, particularly the processing of negative emotions, appears to be a key element in the neurobiology of AN.
With new neuromodulation techniques, specially TMS, it seems possible to modulate the neuronal circuits inherent to emotional processing, such as the L-DLPFC.
Future randomized clinical trials are needed in order to understand how neuromodulation can contribute to exploring the neurobiology of AN and to become more targeted and effective therapeutic options.
Disclosure of InterestNone Declared
Cerebellar dysfunction and autism spectrum disorders – what do we know?
- C. Pinheiro Ramos, M. Alves, J. Marta, R. Ribeiro, A. Gamito
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- Journal:
- European Psychiatry / Volume 66 / Issue S1 / March 2023
- Published online by Cambridge University Press:
- 19 July 2023, p. S239
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Introduction
Autism spectrum disorders (ASD) are complex neurodevelopmental conditions characterized by impairments in social cognition and repetitive behaviors with onset in early infancy. Deficits in emotion recognition, social perception, and communication have been identified as core symptoms of ASD.
Comorbid disorders are frequent, namely psychiatric illness, epilepsy, sleep disruption, and hyperactivity.
Immune profile changes during early life may contribute to pathogenesis of ASD. Other risk factors include advanced parental age, fetal environment, fertility treatments, medications, and nutritional and toxic factors.
Several brain regions are involved in the pathophysiology of ASD but the cerebellum is the structure most consistently found altered. An increased risk of ASD is associated with cerebellar damage.
ObjectivesTo highlight the importance of understanding the key processes of cerebellar development and how altered cerebellar function leads to social and cognitive impairments, and consequently ASD.
MethodsNon-systematic review of the literature using Pubmed database. Papers were selected according to their relevance.
ResultsFrom imaging studies, we can understand that cerebellum is not just about motor function. Different tasks like adding working memory, emotional and social processing, and language seem to be part of core functions of the cerebellar circuit.
Adults with lesions in the cerebellum can develop cerebellar cognitive affective syndrome (CCAS), with core symptoms of impaired executive function, difficulties in spatial cognition, blunted affect, or inappropriate behavior. Some children who have tumor resection surgery for medulloblastomas also exhibit symptoms of CCAS, and some experience posterior fossa syndrome (PFS).
The linguistic, cognitive, and behavioral deficits in CCAS and PFS may contribute to explaining how cerebellar alterations are related to ASD, which is a neurodevelopmental disorder characterized by an earlier onset and broader spectrum of these symptoms.
ConclusionsThe literature has suggested an important role for cerebellar dysfunction in etiology of ASD, under certain premises: (a) cerebellar expansion temporarily coincides with onset of ASD; (b) cerebellum is prone to lesions during this period; (3) cerebellar lesions contribute to dysfunctional social and language abilities.
Disturbances in cerebellar development lead to alterations in higher cognitive functions, due to changes in Purkinje cells. These dysfunctional neurons, once integrated into a brain circuit that controls complex tasks, lead to these functions becoming aberrant.
It is therefore fair to say that cerebellum is important for development of the so-called “cognitive and social brain” since it is itself part of this network. So, the cerebellum certainly plays a relevant role in pathophysiology of ASD.
Disclosure of InterestNone Declared