Pathophysiology is the study of the changes of normal mechanical,physical,and biochemical functions either caused by disease,or resulting from an abnormal syndrome such as: pathophysiology depression,pathophysiology lung cancer, or pathophysiology diabetes
Adhd causes you to not be able to sit for long periods at a time you have to get up and do something,you cant pay attention or focus longer than 5min or less,and you are difficult to be around such as making friends. Treatment has to do with counseling,medication such as ritalin,adderall,concerta,sttratera,vyvanse,and intuniv some therapy maybe. Good luck and i hope this was helpful michelle.
Diagram of the human brain
The pathophysiology of ADHD is unclear and there are a number of competing theories. Research on children with ADHD has shown a general reduction of brain volume, but with a proportionally greater reduction in the volume of the left-sided prefrontal cortex. These findings suggest that the core ADHD features of inattention, hyperactivity, and impulsivity may reflect frontal lobe dysfunction, but other brain regions particularly the cerebellum have also been implicated. Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are only used for research not diagnostic purposes.A 2005 review of published studies involving neuroimaging, neuropsychological genetics, and neurochemistry found converging lines of evidence to suggest that four connected frontostriatal regions play a role in the pathophysiology of ADHD: The lateral prefrontal cortex, dorsal anterior cingulate cortex, caudate, and putamen.
In one study a delay in development of certain brain structures by an average of three years occurred in ADHD elementary school aged patients. The delay was most prominent in the frontal cortex and temporal lobe, which are believed to be responsible for the ability to control and focus thinking. In contrast, the motor cortex in the ADHD patients was seen to mature faster than normal, suggesting that both slower development of behavioral control and advanced motor development might be required for the fidgetiness that characterizes ADHD. It should be noted that stimulant medication itself may affect growth factors of the central nervous system.
The same laboratory had previously found involvement of the "7-repeat" variant of the dopamine D4 receptor gene, which accounts for about 30 percent of the genetic risk for ADHD, in unusual thinness of the cortex of the right side of the brain; however, in contrast to other variants of the gene found in ADHD patients, the region normalized in thickness during the teen years in these children, coinciding with clinical improvement.
Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity), and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain's ability to produce neurotransmitters like dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine (hypodopaminergia) across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to "childhood learning problems" in healthy subjects as well. One interpretation of dopamine pathway tracers is that the biochemical "reward" mechanism works for those with ADHD only when the task performed is inherently motivating; low levels of dopamine raise the threshold at which someone can maintain focus on a task which is otherwise boring. Neuroimaging studies also found that neurotransmitters level (e.g. dopamine and serotonin) in the synaptic cleft goes down during depression.
A 1990 PET scan study by Alan J. Zametkin et al. found that global cerebral glucose metabolism was 8% lower in medication-naive adults who had been hyperactive since childhood. Further studies found that chronic stimulant treatment had little effect on global glucose metabolism,a 1993 study in girls failed to find a decreased global glucose metabolism, but found significant differences in glucose metabolism in 6 specific regions of the brains of ADHD girls as compared to control subjects. The study also found that differences in one specific region of the frontal lobe were statistically correlated with symptom severity. A further study in 1997 also failed to find global differences in glucose metabolism, but similarly found differences in glucose normalization in specific regions of the brain. The 1997 study also noted that their findings were somewhat different than those in the 1993 study, and concluded that sexual maturation may have played a role in this discrepancy. The significance of the research by Zametkin has not been determined and neither his group nor any other has been able to replicate the 1990 results.
Critics, such as Jonathan Leo and David Cohen, who reject the characterization of ADHD as a disorder, contend that the controls for stimulant medication usage were inadequate in some lobar volumetric studies which makes it impossible to determine whether ADHD itself or psychotropic medication used to treat ADHD is responsible for the decreased thickness observed in certain brain regions. While the main study in question used age-matched controls, it did not provide information on height and weight of the subjects. These variables it has been argued could account for the regional brain size differences rather than ADHD itself. They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.
Attention-deficit hyperactivity disorder management
Methods of treatment often involve some combination of behavior modification, life-style changes, counseling, and medication. A 2005 study found that medical management and behavioral treatment is the most effective ADHD management strategy, followed by medication alone, and then behavioral treatment.While medication has been shown to improve behavior when taken over the short term, they have not been shown to alter long term outcomes.
A 2009 review concluded that the evidence is strong for the effectiveness of behavioral treatments in ADHD.
Psychological therapies used to treat ADHD include psychoeducational input, behavior therapy, cognitive behavioral therapy (CBT), interpersonal psychotherapy (IPT), family therapy, school-based interventions, social skills training and parent management training.
Parent training and education have been found to have short term benefits. Family therapy has shown to be of little use in the treatment of ADHD, though it may be worth noting that parents of children with ADHD are more likely to divorce than parents of children without ADHD, particularly when their children are younger than eight years old.
Several ADHD specific support groups exist as informational sources and to help families cope with challenges associated with dealing with ADHD.
A 2009 study found that children with ADHD move around a lot because it helps them stay alert enough to complete challenging tasks. The researcher advises that when they are doing homework, one should let them fidget, stand or chew gum since it may help them cope. Unless their behavior is destructive, severely limiting their activity could be counterproductive.
Management with medication was shown to be the most cost-effective, followed by behavioral treatment and combined treatment in a 14 month follow-up study. However, a follow-up study found that stimulant medication offered no benefits over behavioral therapy in children after their respective treatments allocations had been discontinued for two years. Stimulant medication or non-stimulant medication may be prescribed. A 2007 drug class review found that there are no good studies of comparative effectiveness between various drugs for ADHD and that there is a lack of quality evidence on their effects on overall academic performance and social behaviors. ADHD medications are not recommended for preschool children as their long term effects in such young people are unknown.There is very little data on the long-term adverse effects or benefits of stimulants for ADHD.
Ritalin 10 mg tablets (AU)
Stimulants are the most commonly prescribed medications for ADHD. The most common stimulant medications are the chain subsitituted amphetamine methylphenidate (Ritalin, Metadate, Concerta), dextroamphetamine (Dexedrine), mixed amphetamine salts (Adderall),dextromethamphetamine (Desoxyn) and lisdexamfetamine (Vyvanse). However, caution needs to be used when prescribing medications that increase levels of "feel-good" neurotransmitters like dopamine, because they can be addictive (see article: amphetamine dependence).According to several studies, use of stimulants (e.g. methylphenidate) can lead to development of drug tolerance to therapeutic doses; tolerance also occurs among high dose abusers of methylphenidate.
Stimulants used to treat ADHD raise the extracellular concentrations of the neurotransmitters dopamine and norepinephrine which causes an increase in neurotransmission. The therapeutic benefits are due to noradrenergic effects at the locus coeruleus and the prefrontal cortex and dopaminergic effects at the nucleus accumbens.
A meta analysis of clinical trials found that about 70% of children improve after being treated with stimulants in the short term but found that this conclusion may be biased due to the high number of low quality clinical trials in the literature. There have been no randomized placebo controlled clinical trials investigating the long term effectiveness of methylphenidate (Ritalin) beyond 4 weeks. Thus the long term effectiveness of methylphenidate has not been scientifically demonstrated. Serious concerns of publication bias regarding the use of methylphenidate for ADHD has also been noted.
Higher rates of schizophrenia and bipolar disorder as well as increased severity of these disorders occur in individuals with a past history of stimulant use for ADHD in childhood.
Emergency room visits by children ages 10–14 involving Ritalin intoxication have now reached the same level as those for cocaine which indicates escalating abuse of this highly addictive drug. US and Canada account for a startling 95 percent of worldwide Ritalin consumption. In one study which looked at adult cocaine users, it was found that those individuals who used Ritalin between one and ten years of age had a percentage of cocaine abuse twice that of those who had been diagnosed with ADHD but had not utilized Ritalin
Both children with and without ADHD abuse stimulants, with ADHD individuals being at the highest risk of abusing or diverting their stimulant prescriptions. Between 16 and 29 percent of students who are prescribed stimulants report diverting their prescriptions. Between 5 and 9 percent of grade/primary and high school children and between 5 and 35 percent of college students have used nonprescribed stimulants. Most often their motivation is to concentrate, improve alertness, "get high," or to experiment.
Although one review indicates that long-term use of methylphenidate has potential for abuse and addiction due to its similar pharmacologically to cocaine and amphetamines, the use of stimulant therapy for ADHD does not increase the risk of subsequent substance abuse and may be protective against it when treatment is started in childhood. However, when stimulant therapy is started during adolescence or adulthood, there is an increased risk of subsequent substance abuse.
One study found that children with ADHD actually need to move more to maintain the required level of alertness while performing tasks that challenge their working memory. Performing math problems mentally and remembering multi-step directions are examples of tasks that require working memory, which involves remembering and manipulating information for a short time. These findings may also explain why stimulant medications improve the behavior of most children with ADHD. Those medications improve the physiological arousal of children with ADHD, increasing their alertness. Previous studies have shown that stimulant medications temporarily improve working memory abilities.
Although "under medical supervision, stimulant medications are considered safe", the use of stimulant medications for the treatment of ADHD has generated controversy because of undesirable side effects, uncertain long term effects and social and ethical issues regarding their use and dispensation. The FDA has added black-box warnings to some ADHD medications, while the American Heart Association and the American Academy of Pediatrics feel that it is prudent to carefully assess children for heart conditions before treating them with stimulant medications.
A novel stimulant drug that has been used to treat ADHD is modafinil. There have been double-blind randomized controlled trials that have demonstrated the efficacy and tolerability of modafinil, however there are risks of serious side effects such as skin reactions and modafinil is not recommended for use in children.
Risperdal 4 mg tablets (UK)
In an odd contrast with the approved use of stimulant medication as a treatment for children with ADHD, the use of atypical antipsychotic drugs as an off-label treatment has been rising.
Antipsychotics work by blocking dopamine, whereas stimulants trigger its release. Atypical antipsychotics have been approved for use in children and teenagers with schizophrenia spectrum disorders and autistic spectrum disorders by the U.S. Food and Drug Administration (FDA) since 1993.
Atypical antipsychotics are not theoretically suitable for treating children with ADHD. As consistently demonstrated in clinical stimulant trials, and biological brain imaging in ADHD subjects, the dopamine hypothesis has in more recent times become accumulative evidence, strongly linking under-stimulated dopaminergic neurotransmission as an etiologic cause of ADHD. Children who have ADHD and respond to stimulant medication experience a paradoxical effect; instead of becoming over-stimulated like a non-ADHD child, the inhibitory pathways of their brain are stimulated, therefore they subsequently become calmer, less prone to hyperactivity, not as easily distracted or impulsive, are able to focus, and academically perform at a level that isn't indifferent from other non-ADHD children. On the other hand, treatment with antipsychotic medications may ostensibly provide an ADHD child who doesn't respond well to stimulants with similar effects on behavior, however, their cognitive dysfunction and inability to focus have been further exacerbated. Non-ADHD children do not respond in a dissimilar way to ADHD children when prescribed antipsychotic drugs, which are also less commonly prescribed off-label for aggression in children. The ADHD child on antipsychotic drugs is not calmer like the ADHD child on stimulant drugs, they're sedated, or tranquilized. The pressure, which may come from both at school and at home to control the ADHD child's disruptive behavior is likely to have diverted attention away from what is in the child's best interest.
Careful approach needs to be taken when blocking dopamine function, which is responsible for the psychological reward system. Excessive blocking of this neurotransmitter can cause dysphoria. This may in turn cause suicidal ideation, or lead some teenagers to compensate for their dopamine deficiency with illicit drugs or alcohol. Atypical antipsychotics are preferred for this reason, because they are less likely to cause movement disorders, dysphoria, and increased drug cravings that have been associated with older typical antipsychotics.Weight gain, diabetes, lactation, gynecomastia, drooling, dysphoria, anhedonia (inability to experience pleasure), fatigue, sexual dysfunction, heart rhythm problems and the possibility of tardive dyskinesia, an irreversible movement disorder, are among the adverse events associated with antipsychotic drugs.
Other non-stimulant medications
Atomoxetine (Strattera) and Guanfacine (Intuniv) are the only non-stimulant drugs approved for the treatment of ADHD. Other medications which may be prescribed off-label include α2A adrenergic receptor agonists such as clonidine, certain antidepressants such as tricyclic antidepressants, SNRIs, SSRIs or MAOIs.
I hope I have been of help.
Take care and have a good day.
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