View Full Version : Treat Symptoms or Treat Diagnoses?


psychological1
06-30-14, 12:29 PM
I brought up this question somewhere on another thread, but I would like to hear some other people's opinions.

The question is regarding two fundamental approaches to psychiatric care. The prevailing approach today posits that, when a patient seeks care with a psychiatrist, they evaluate the patient in detail and assign a specific diagnosis. This diagnosis is then treated based on literature that states a standard treatment plan for diagnosis X. Most of the time, this system works well. It standardizes treatment and diagnoses, allowing for consistent care shown to be beneficial. This system can be called "treating the diagnosis."

Some psychiatrists prefer to take a slightly different approach when the case of the patient isn't so cut and dry. Like in the thread started by Michigan (and many other people with similar problems), their symptoms may cause significant impairment in normal functioning, but they don't quite qualify for a specific diagnosis. Does this mean that they shouldn't receive treatment? They don't qualify by the standardized system for a diagnosis, but their symptoms may be significant. Consider a situation where a person has a diagnosis of bipolar disorder. They are treated with lithium, and soon that person develops psychotic symptoms. The doctors decides to add an antipsychotic medication to treat these symptoms, even thought the primary diagnosis is still bipolar. This approach looks at each symptom the patient presents, and develops a treatment plan that focuses on the symptoms, rather than the diagnostic category.

The goal of seeking treatment is to reduce the symptoms that impair normal functioning. The field of psychiatry is unique in that the biological understanding of mental disorders is very crude. Because of this, we can't place every patient in a lumped category with a standard treatment regimen, as identical symptoms may manifest from biologically unrelated causes; researchers simply do not know.

This article better articulates what I'm discussing:

http://www.kevinmd.com/blog/2011/05/psychiatry-treat-symptoms-diseases.html

I recommend giving it a read (it's short)!

sarahsweets
07-01-14, 07:41 AM
I am not against treating the symptoms but only if every possible cause has been Exhausted. And I mean really exhausted because so many things mimic each other its important to find the most likely cause. Its sort of like treating pain medication. Sure, pain is a symptom and no one should suffer but finding the source or cause of the pain is just as important as treating it. Pain medication is rarely recommended for long term daily use ( i say rarely but there some people that just cant function without it.)

psychological1
07-01-14, 09:51 AM
I am not against treating the symptoms but only if every possible cause has been Exhausted. And I mean really exhausted because so many things mimic each other its important to find the most likely cause. Its sort of like treating pain medication. Sure, pain is a symptom and no one should suffer but finding the source or cause of the pain is just as important as treating it. Pain medication is rarely recommended for long term daily use ( i say rarely but there some people that just cant function without it.)

Yes that is a good point. I'm speaking mostly about those cases that don't quite fit a single diagnosis. If it is possible to pinpoint, then treating the cause is really the same thing as treating the symptoms; they both will have the same outcome. But it seems that often, doctors are too focused on finding a specific diagnosis when one may just never be found. Meanwhile, many medications exist for the symptoms people experience, but doctors won't administer it because they don't fit within the parameters. I think that ADHD symptoms often fall into that category.

mildadhd
07-01-14, 02:26 PM
I find understanding ADHD, biologically, from the ground up and being primarily an overactive SEEKING system, the most helpful and easiest to understand.

..The DSM IV defines attention deficit disorder by its external features, not by its emotional meaning in the lives of individual human beings.

It commits the faux pas of calling these external observations symptoms, whereas that word in medical language denotes a patient's own felt experience.

External observations, no matter how acute, are signs.

A headache is a symptom.

A chest sound registered by the doctor's stethoscope is a sign.

A cough is both a symptom and a sign.

The DSM speaks the language of signs because the worldview of conventional medicine is unfamiliar with the language of the heart..

..ADD has much to do with pain, present in every one of the adults and children who have come to me for assessment.

The deep emotional hurt they carry is telegraphed by the downcast, averted eyes, the rapid, discontinuous flow of speech, the tense body postures, the tapping of feet and fidgety hands and by the nervous, self-deprecating humor.

"Every aspect of my life hurts," a thirty-seven-year-old man told me during his second visit to my office.

People express surprise when after a brief exchange I seem to be able to sense their pain and grasp their confused and conflicted history of emotions.

"I'm speaking about myself," I tell them.

At times I have wished that the "experts" and media pundits who deny the existence of attention deficit disorder could meet only a few of the severely affected adults who have sought my help.

These men and women, in their thirties, forties and fifties, have never been able to maintain any sort of a long-term job or profession.

They cannot easily enter meaningful, committed relationships, let alone stay in one.

Some have never been able to read a book from cover to cover, some cannot even sit through a movie.

Their moods fly back and forth from lethargy and dejection to agitation.

The creative talents they have been blessed with have not been pursued.

They are intensely frustrated at what they perceive as their failures.

Their self-esteem is lost in some deep well.

Most often they are firm in the conviction that their problems are the result of a basic, incorrigible flaw in their personalities.


-Gabor Mate M.D., "Scattered", P 8-9.


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daveddd
07-01-14, 07:01 PM
symptoms


technically all mental disorders are nothing more than exclusionary symptoms

if that wasn't the case your dx will look like this

example- adhd , due to traumatic brain injury

autism- due to rett syndrome

mildadhd
07-02-14, 02:11 PM
Indicators and Neuroanatomy of ADHD

It is commonly thought that, beside various environmental influences, the genesis of ADHD involves diverse gene expression patterns each with small individual effects (Tripp & Wickens, 2009).

The visible indicators of ADHD, occurring either individually or in any combination, include most prominently the inability to maintain focus or attention for longer periods of time, hyperactivity and diminished impulse control.

Children with ADHD may also exhibit aggressive behaviors, and hence be diagnosed with comorbid disorders such as Conduct Disorder and Oppositional Defiant Disorder.

Peer Relationships

As may be expected, children with ADHD have more difficulty with peer relationships than children without ADHD.

In a study of 165 children (7-9 years) with ADHD, Hoza et al (2005) found that these children had fewer friendships and were viewed negatively by peers.

Indeed, 52% of the children studied fell into the rejected category based on measures of “social preference”, “social impact” and “liking”.

Their lack of social success appears to be due, at least in part, to problems interpreting and responding to social cues.

Andrade et al. (2012) found that, when compared with controls, children with ADHD and Conduct Problems i) tended to miss social cues (possibly due to inattention or working memory deficits), ii) interpret intentions of others and outcomes of interactions differently (both more positively or more negatively), and iii) often exhibit more negatively valenced responses to negative social situations (whereas, controls tended to exhibit more positive responses, even in negative situations).

Thus, the social awkwardness, misinterpretations and mistakes made by children with ADHD often results in social neglect or outright rejection by peers, which obviously amplifies social problems.

The quality of friendships and peer relationships or lack thereof have long-term effects as children mature into adults.

Childhood rejection by peers is predictive of negative behaviors (e.g., delinquency, substance abuse, dropping out of school, criminal activity) and feelings (e.g., depression, loneliness, anxiety (Parker and Asher, 1987; Rubin et al., 1998).

However, it is important to remember that these results are not due to rejection alone; many other factors such as peer group choice come into play.


ADHD Endophenotypes

Castellanos and Tannock (2002) have identified three potential neuroscience-based endophenotypes that involve the executive functions of the brain.

1) Hyperactive behavior may be a result of a shortened delay gradient, which decreases the time one is willing to wait for a reward (e.g., recess, food treat, money, etc.).

They hypothesize that fidgeting or hyperactivity may reflect a self-regulatory behavior when waiting is enforced.

2) Waiting, even for short times, may be extra difficult for people with ADHD because of differences in temporal processing that skew perceptions of time.

Deficits in temporal processing may also be responsible for inattentive behaviors and inconsistent performance often seen in people with ADHD.

3) The final proposed endophenotype reflects a working memory deficit that affects executive functions (including impulse control), ability to maintain attention/focus, and even phonemic awareness deficits (e.g., dyslexia).

Deficits in working memory may also promote the shortened reward-delay gradient that characterizes ADHD.


Neuroanatomy of ADHD

MRI monitored brain structural comparisons of children with ADHD and children without ADHA have produced conflicting results but some general conclusions can be made.

In their review of recent studies, Krain and Castellanos (2006), report a 3.2-4% reduction in overall ADHD brain size, including especially reductions in the frontal, parietal, temporal and occipital lobes.

However, differences in the frontal lobe, especially the prefrontal cortex (PFC), account for most of this reduction. Significant reductions have also been found in the cerebellum, an area involved in motor, timing, and attentional functions.

Krain and Castellanos describe grey and white matter volume differences, both reductions and increases, in the PFC as well as many other brain areas.

Variations have also been found in the size and asymmetry of the caudate nucleus and volume of the putamen but results are less consistent in these areas.

It is important to note that some of these brain differences are found in young children but are no longer seen in adolescence (e.g., caudate volumes seem to normalize around age 16).

It is generally believed that ADHD reflects deficits in brain dopamine transmission; solid evidence for that is lacking (Tripp & Wickens, 2009) but clearly dopamine influences need to be considered in the context of other brain neurochemical patterns (Oades, 2008).

Thus, researchers have not been able to conclude that any of these brain variations are causal factors for ADHD behaviors, though neural correlations with response inhibition, impulsivity, hyperactivity, and attention have been found.

http://www.scholarpedia.org/article/ADHD_and_Play

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mildadhd
07-02-14, 02:25 PM
Bold by Peripheral.

REVIEW

Neuroscience of attention-deficit/hyperactivity disorder: the search for endophenotypes

F. Xavier Castellanos & Rosemary Tannock

Abstract
Research on attention-deficit/hyperactivity disorder (ADHD), a highly prevalent and controversial condition, has, for the most part, been descriptive and atheoretical.

The imperative to discover the genetic and environmental risk factors for ADHD is motivating the search for quantifiable intermediate constructs, termed endophenotypes.

In this selective review, we conclude that such endophenotypes should be solidly grounded in the neurosciences.

We propose that three such endophenotypes — a specific abnormality in reward-related circuitry that leads to shortened delay gradients, deficits in temporal processing that result in high intrasubject intertrial variability, and deficits in working memory — are most amenable to integrative collaborative approaches that aim to uncover the causes of ADHD.




(See full link)http://www.med.nyu.edu/research/pdf/castef01-Castellanos%20Tannock%20NRN%202002.pdf



Example:

FIGURE 1 | Causal model of shortened delay gradient as a candidate endophenotype.

http://www.nature.com/nrn/journal/v3/n8/images/nrn896-f1.gif

http://www.nature.com/nrn/journal/v3/n8/fig_tab/nrn896_F1.html


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mildadhd
07-02-14, 03:45 PM
See More Figures and Tables (http://www.nature.com/nrn/journal/v3/n8/fig_tab/nrn896_ft.html)

Example

FIGURE 2 | Selective BOLD fMRI activation during anticipation of a monetary reward.

http://www.nature.com/nrn/journal/v3/n8/images/nrn896-f2.gif

Selective activation was found in the nucleus accumbens (NAcc) and the anterior cerebellar vermis (Cb) of eight normal adults in a study using blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI)69. The colours indicate the statistical significance of those regions that responded during the anticipation of $5.00 versus $0.20. The caudate, thalamus and posterior cingulate were also activated. Image courtesy of B. Knutson, Stanford University.



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