Case Study Of Antidepressant Patients

Lastly, what effects to antidepressants have on mood, behavior, and suicidal tendencies? In her article, ‘The Hidden Harm of Antidepressants’, Diana Kwon, a science writer with a Master’s degree for McGill University in neuroscience, she reviews several studies about the use of antidepressants, and had found the safety data on some of these drugs have been withheld from the public. She mentions research done in Copenhagen by some researchers at the Nordic Cochrane Center, and how they discovered that “pharmaceutical companies were not presenting the full extent of serious harm in clinical study reports…” (Kwon para 2). These clinical study reports are then used by people at the U.S. Food and Drug Administration (FDA) to approve or deny new

It’s simply easy to discard a young adult with a hint of depression or anxiety in society’s eyes. In fact, depression is a fickle box, a diverse illness, with different prior causes and abstract theories (Mukherjee, New York Times Magazine, 2012). Most adults might be under a false impression that it’s a normal for children to have severe mood swings. As for the adults who have worked under the physiatric/medical field, knew professionally that wasn’t the case. Antidepressants is the key ingredient and solution for these young adults to handle for their own mental problems. Con: However, The U.S Food and Drug Administration slapped “black box” warning on antidepressants, with even a small minority chance of increased suicide risk, behind the agency's strongest safety alert (Olson, Omaha World-Herald, 2005).

Antidepressants have a history of causing violent side effects, including suicide and homicide in those consuming the prescribed drugs. Many antidepressants that are prescribed to those with a mental illness come packaged with a warning label that reads: “New or worsening depression; thinking about harming or killing yourself, or planning or trying to do so; extreme worry; agitation; panic attacks; difficulty falling asleep or staying asleep; aggressive behavior; irritability; acting without thinking; severe restlessness; and frenzied abnormal excitement." This warning label is a most know for school officials who are aware of students dealing with a mental illness. Statistics show that five of the top 10 most violence-inducing drugs were found

Research Question: Are antidepressants being over prescribed, if so what other options do doctors have and what should they be considering?

An excess in dopaminergic, and a deficit in glutaminergic (specifically NMDA) signalling correspond to positive and negative symptoms respectively. The NMDA antagonist MK-801 is used in animal models of schizophrenia, while paranoid and persecutory delusions are typical of methamphetamine users. In those with an

When antidepressant medication is advertised, benefits and negative side effects are provided, but what is not informed to the consumer is how it actually works. The truth behind antidepressant pills is that they don’t kick in right away and may take four to six weeks before they reach their full therapeutic effect. Many also find that it takes several trials before finding the one that works (Smith). This process can be long, strenuous, and costly. Additionally, a large portion of those who try pills in the end find that they are treatment-resistant to the medication, meaning all their efforts were a waste. There exists another form of resistance as well considered “depressive breakthrough” which is defined as the return of depressive symptoms

Other adjuvent medications have shown efficacy for the treatment of NP in either a single RCT or inconsistently across multiple RCTs. These medications should be reserved for patients who cannot tolerate or who do not respond adequately to first- and second-line medications. These medications include certain antidepressant medications (eg, bupropion, citalopram, and paroxetine), certain antiepileptic medications (eg, carbamazepine, lamotrigine, topiramate, and valproic acid), dextromethorphan, memantine, mexiletine and topical low-concentration Capsaicin (Qutenza) 8% (concentrated extract of chili peppers)

As the human brain evolved to encompass higher order functions, this increased cortical activity lead to increased metabolic demands. Broadly speaking, these heightened metabolic demands created energetic stressors in the brain, thereby amplifying the negative consequences of synaptic plasticity and demyelination in the human brain and making it more susceptible to

ERD has been observed during cognitive and attentional tasks (Dujardin et al., 1993). ERD is expected to be useful in clinical practice as an index reflecting abnormal cognitive functions specific to neurological and psychiatric

Most notable diseases include Parkinson's, Schizophrenia, depression, and ADHD. These diseases occur when the dopamine levels in the brain are imbalanced. Schizophrenia occurs when a person's brain has an exorbitant amount of dopamine. This is also the case with other mental diseases such as bipolar disorder. Treatment usually includes a medication with a dopamine inhibitor, which limits the pace of dopamine transferring from one neuron to another. On the opposite end of the spectrum, diseases such as ADHD and depression are associated with lack of dopamine production (Alban 2017). Parkinson's is caused by the degeneration of the parts of the brain that manufacturer's dopamine (2017). All of these diseases are tremendously critical and should not be taken

Both structural and functional changes in the brain activity are considered the underlying pathophysiology of the disease (9).

The basal ganglia is organized and functionally segregated that is critical for motor, sensorimotor, and cognitive (Natarajan & Yamamoto, 2011). Basal ganglia dysfunctions are associated with cognitive motor, Parkinson’s, Huntington’s, Tourette’s syndrome, and obsessive compulsive disorder. The major input in the basal ganglia us the striatum, which is divided into dorsal and ventral regions. Basal ganglia function is related to the action of the amphetamines and other psychostimulant drugs of abuse (Natarajan & Yamamoto,

with ASD (Baron-Cohen, 1988; Dewey & Everard, 1974; Kim et al., 2014; Tager-Flusberg, 1981; Volkmar,

Glutaric aciduria is an inherited autosomal recessive condition in which the body is incapable of completely processing proteins. This is due to mutations of the GCDH gene which is involved in the production of glutaryl-CoA dehydrogenase which in turn is involved in processing the building blocks of proteins; amino acids. The enzyme glutaryl-CoA dehydrogenase is responsible for processing the amino acids lysine, hydroxylysine, and tryptophan. With the body unable to process these amino acids, they build to toxic levels and attack the basal ganglia portion of the brain forming irreparable damage. The basal ganglia is responsible for regulating both voluntary and involuntary muscle movement, learning, cognition, and emotion. To the casual

Although single voxel MRS generates spectra with high signal-to-noise ratio, a single MRS voxel cannot be placed in a homologous brain region because of differing brain size and gray matter gyration across individuals. Furthermore, an MRS voxel across participants will contain differing amounts of gray and white matter, with each tissue type containing differing amounts of metabolites will contribute differentially to MRS signal. Therefore, variability in placement and amounts of differing tissue types increases variability in metabolite levels ascertained from single voxel MRS, decreasing statistical power to detect abnormalities in metabolite levels. Second, extant studies often used a case-control design where MR data were acquired only once in each participant. These studies therefore can assess only associations, but not causal relations, between metabolite levels and mechanism of illness. Third, although treatment response and symptoms across unipolar depression fall along a continuum, abnormalities in brain structure, function, and metabolism in DD may differ from those in MDD. Brain abnormalities in DD therefore cannot be inferred from studies of MDD. For example, we showed23 that individuals at high risk for MDD compared with those at low risk had thinner cortex in the right hemisphere of the brain, whereas patients with DD had thicker cortex across large portions of the brain24. Similarly, metabolic abnormalities in