Seminar

Attention-deficit hyperactivity disorder and hyperkinetic disorder

Psychiatric and cognitive comorbidities have been known to play a major role in human epilepsy for a long time. People with epilepsy (PWE) frequently express signs of varying psychiatric and cognitive disorders affecting their quality and quantity of life (QoL/QaoL). Over the last few years, research on behavioural comorbidities and their effect on the underlying disease have been performed in canine epilepsy. The following article reviews manifestations of comorbidities in canine epilepsy with an emphasis on patterns of clinical signs and their effects on QoL and QaoL. Cognitive and behavioural alterations in epileptic dogs are mainly represented by fear-/anxiety related behaviour and cognitive impairment (CI). Reduced trainability and altered reactions to daily situations are common results of comorbid changes posing obstacles in everyday life of owners and their dog. In addition, clinical signs similar to attention deficit hyperactivity disorder (ADHD) in humans have been reported. Canine attention-deficit-hyperactivity-disorder-like (c-ADHD-like) behaviour should, however, be evaluated critically, as there are no official criteria for diagnosis of ADHD or ADHD-like behaviour in dogs, and some of the reported signs of c-ADHD-like behaviour could be confused with anxiety-associated behaviour. Many intrinsic and extrinsic factors could potentially influence the development of behavioural and cognitive comorbidities in canine epilepsy. In particular, seizure frequency/severity, signalment and factors concerning disease management, such as pharmacotherapy and nutrition, are closely linked with the presence of the aforementioned comorbid disorders. Further studies of behavioural alterations in epileptic dogs are needed to comprehend the complexity of clinical signs and their multifactorial origin.

Person-oriented analyses are commonly used to identify subgroups of children with mental health conditions in the hopes that they will meaningfully inform the taxonomy, assessment, and treatment of psychological disorder. However, whether these data-driven groups are demonstrably better at predicting important aspects of adaptive functioning than standard DSM taxonomy has not been established. Using Attention-Deficit-Hyperactivity-Disorder (ADHD) as a model condition, we utilized dimensions of personality and cognitive ability to identify person-centered profiles of school-aged children (N=246) and evaluated the association of these profiles with critical areas of adaptive functioning. A single profile (“Conscientious”) represented non-ADHD controls and was characterized by faster drift rate and higher executive functioning scores. Three profiles (“Disagreeable,” “Negative Emotionality,” and “Extraverted”) were identified for children with ADHD. Drift rate, but not executive functioning, distinguished among ADHD profiles, which were also distinctly associated with comorbid externalizing and internalizing psychopathology, social skills, and academic achievement. In contrast, the Diagnostic and Statistical Manual (DSM) presentations were not informative and showed similar patterns of impairment across domains. Person-centered profiles of children with ADHD are associated with distinct adaptive functioning deficits and may be useful in informing clinical practice.

Aggressive driving is known to be a cause of vehicle accidents. Individuals with Attention-deficit hyperactivity disorder (ADHD) are prone to more aggressive behavior and that also leads to aggressive driving. To prevent aggressive driving, we strive to first understand aggressive driving and find patterns in this type of driving behavior. In an effort to uncover to identify patterns in aggressive driving, we examine sensor data and video data of trips taken by drivers with ADHD and identify our distinct aggressive driving patterns. Using the sensor data, we extend our findings to all aggressive trips in our dataset and generate a model to detect aggressive driving patterns. By finding the similarity between trips and then using these distances to produce a KNN model, we are able to model our data and classify it into 4 driving patterns. This analysis can better inform us of the type of driving patterns that appear in aggressive driving. Using this analysis, we can also better understand which patterns are produce better precision and recall using this methodology.

Attention deficit hyperactivity disorder (ADHAD) is a neurobehavioral disorder that affects children and adolescents with a high prevalence. Despite its prevalence and an unclear etiology, previous reports suggest that it is closely related to homocysteine metabolism. Male Sprague Dawley rats were administered with homocysteine from postnatal day (PD) 2 to PD 16. Locomotor activity was evaluated at 35 PD (prepuberal age) and 60 PD (adult age) before and after amphetamine administration. In rats evaluated at both ages, homocysteine induced hyperactivity, and the amphetamine administration reduced hyperactivity significantly at 35 PD, but not at 60 PD. In the social interaction test, homocysteine reduced the number of contacts and increased the latency to the first contact only in rats at 35 PD. Homocysteine also had an effect on short term memory at 35D and 60 PD and long-term memory at 60 PD. Morphological changes were found mainly in the shape of dendritic spines in the prefrontal cortex (PFC-3), dorsal hippocampus (CA1), dentate gyrus (DG) and nucleus accumbens (NAcc), in rats administered neonatally with homocysteine at both ages studied. In prepuberal and adult rats, there was an increase in dendritic length in DG and NAcc, respectively. The dendritic spine morphology also was altered at both ages, mainly decreasing the number of mushroom spines in NAcc and CA1 at 30 PD and in all the areas studied at 60 PD rats. Those areas are associated with the processes of attention, learning and memory that were studied, and those alterations are possibly related to changes observed in the behavioral tests. These behavioral and morphological changes in rats at 35 PD administered with homocysteine could be similar to changes found in children diagnosed with ADHD. Moreover, half to two thirds of children diagnosed with ADHD reach adulthood with this disorder. In this study we found similarities with ADHD, finding alterations in both rats at 35 PD and 60 PD. So, this may be proposed as an animal model to study this disorder present in children, adolescents and adults.