Appendicular Skeleton

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Appendicular Skeleton

The appendicular skeleton is composed of 126 bones in the human body. The word appendicular is the adjective of the noun appendage which itself means a part that is joined to something larger. Functionally it is involved in locomotion (Lower limbs) of the axial skeleton and manipulation of objects in the environment (Upper limbs).

The appendicular skeleton is divided into six major regions:

1) Pectoral Girdles (4 bones) – Left and right Clavicle (2) and Scapula (2).

2) Arm and Forearm (6 bones) – Left and right Humerus (2) (Arm), Ulna (2) and Radius (2) (Fore Arm).

3) Hands (58 bones) – Left and right Carpal (16) (wrist), Metacarpal (10), Proximal phalanges (10), Middle phalanges (8), distal phalanges (10), and sesamoid (4).

4) Pelvis (2 bones) – Left and right os coxae (2) (ilium).

5) Thigh and leg (8 bones) – Femur (2) (thigh), Tibia (2), patella (2) (knee), and Fibia (2) (leg).

6) Feet (48) – Tarsals (14) (ankle), Metatarsals (10), Proximal phalanges (10), middle phalanges (8), distal phalanges (10), and sesamoid (4).

It is important to realize that through anatomical variation it is common for the skeleton to have many extra bones (sutural bones in the skull, cervical ribs, lumbar ribs and even extra lumbar vertebrae)

The appendicular skeleton of 126 bones and the axial skeleton of 80 bones together form the complete skeleton of 206 bones in the human body. The appendicular part of the skeleton is unfused unlike the axial of the skeleton this makes movement alot easier. [1]
References:

  1. Vizniak, N.A., 2008, Quick Reference Clinical Consultant Muscle Manual, Professional Health Systems Inc, Canada
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What I Needed to Know about GERD, GORD and Acid Reflux

Gastroesophageal reflux disease (GERD), gastro-oesophageal reflux disease (GORD), gastric reflux disease, or acid reflux disease is defined as chronic symptoms or mucosal damage produced by the abnormal reflux in the esophagus. [1]

This is commonly due to transient or permanent changes in the barrier between the esophagus and the stomach. This can be due to incompetence of the lower esophageal sphincter, transient lower esophageal sphincter relaxation, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia. Respiratory and laryngeal manifestations of GERD are commonly referred to as extraesophageal reflux disease (EERD).

Signs and Symptoms

The most-common symptoms of GERD are:

  • Heartburn
  • Regurgitation
  • Trouble swallowing (dysphagia)

Less-common symptoms include:

  • Pain with swallowing (odynophagia)
  • Excessive salivation (this is common during heartburn, as saliva is generally slightly basic[2] and is the body’s natural response to heartburn, acting similarly to an antacid)
  • Nausea[3]
  • Chest pain

GERD sometimes causes injury of the esophagus. These injuries may include:

  • Reflux esophagitis—necrosis of esophageal epithelium causing ulcers near the junction of the stomach and esophagus.
  • Esophageal strictures—the persistent narrowing of the esophagus caused by reflux-induced inflammation.
  • Barrett’s esophagus—metaplasia (changes of the epithelial cells from squamous to columnar epithelium) of the distal esophagus.
  • Esophageal adenocarcinoma—a rare form of cancer.[3]

Several other atypical symptoms are associated with GERD, but there is good evidence for causation only when they are accompanied by esophageal injury. These symptoms are:

  • Chronic cough
  • Laryngitis (hoarseness, throat clearing)
  • Asthma
  • Erosion of dental enamel
  • Dentine hypersensitivity
  • Sinusitis and damaged teeth[4]

Some people have proposed that symptoms such as pharyngitis, sinusitis, recurrent ear infections, and idiopathic pulmonary fibrosis are due to GERD; however, a causative role has not been established. [3]

Diagnosis

A detailed historical knowledge is vital for an accurate diagnosis. Useful investigations may include ambulatory esophageal pH Monitoring, barium swallow X-rays, esophageal manometry, and Esophagogastroduodenoscopy (EGD). The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and it also allows monitoring GERD patients in regards of their response to medical or surgical treatment. In general, an EGD is done when the patient either does not respond well to treatment or has alarm symptoms including dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate either once-in-a-lifetime or 5/10-yearly endoscopy for patients with longstanding GERD, to evaluate the possible presence of dysphasia or Barrett’s esophagus, a precursor lesion for esophageal adenocarcinoma. [7]

Biopsies can be performed during gastroscopy and these may show:

  • Edema and basal hyperplasia (non-specific inflammatory changes)
  • Lymphocytic inflammation (non-specific)
  • Neutrophilic inflammation (usually due to reflux or Helicobacter gastritis
  • Eosinophilic inflammation (usually due to reflux)
  • Goblet cell intestinal metaplasia or Barretts esophagus
  • Elongation of the papillae
  • Thinning of the squamous cell layer
  • Dysphasia or pre-cancer
  • Carcinoma

Reflux changes may be non-erosive in nature, leading to the entity “non-erosive reflux disease”.

Pathophysiology

GERD is caused by a failure of the cardia. In healthy patients, the “Angle of His”—the angle at which the esophagus enters the stomach—creates a valve that prevents duodenal bile, enzymes, and stomach acid from traveling back into the esophagus where they can cause burning and inflammation of sensitive esophageal tissue.

Another paradoxical cause of GERD-like symptoms is not enough stomach acid (hypochlorhydria). The valve that empties the stomach into the intestines is triggered by acidity. If there is not enough acid, this valve does not open, and the stomach contents are churned up into the esophagus. However, there is still enough acidity to irritate the esophagus.

Factors that can contribute to GERD:

  • Hiatal hernia, which increases the likelihood of GERD due to mechanical and motility factors.[8]
  • Obesity: increasing body mass index is associated with more severe GERD. [9]. In a large series of 2000 patients with symptomatic reflux disease, it has been shown that 13 % of changes in esophageal acid exposure is attributable to changes in body mass index.[10]
  • Zollinger-Ellison syndrome, which can be present with increased gastric acidity due to gastrin production
  • Hypercalcemia, which can increase gastrin production, leading to increased acidity
  • Scleroderma and systemic sclerosis, which can feature esophageal dysmotility
  • The use of medicines such as prednisolone
  • Visceroptosis or Glénard syndrome, in which the stomach has sunk in the abdomen upsetting the motility and acid secretion of the stomach.

GERD has been linked to a variety of respiratory and laryngeal complaints such as laryngitis, chronic cough, pulmonary fibrosis, earache, and asthma, even when not clinically apparent. These atypical manifestations of GERD are commonly referred to as extraesophageal reflux disease.
Factors that have been linked with GERD but not conclusively:

  • Obstructive sleep apnea[11][12]
  • Gallstones, which can impede the flow of bile into the Duodenum, which can affect the ability to neutralize gastric acid

In 1999, a review of existing studies found that, on average, 40% of GERD patients also had H. pylori infection.[13] The eradication of H. pylori can lead to an increase in acid secretion,[14] leading to the question of whether H. pylori-infected GERD patients are any different than non-infected GERD patients. A double-blind study, reported in 2004, found no clinically significant difference between these two types of patients with regard to the subjective or objective measures of disease severity. [15]

Treatment

Dietary modification

Certain foods and lifestyle are considered to promote gastroesophageal reflux, but a 2006 review suggested that evidence for most dietary interventions is anecdotal; only weight loss and elevating the head of the bed were supported by evidence. [16] A subsequent randomized crossover study showed benefit by avoiding eating two hours before bedtime. [8]

The following may exacerbate the symptoms of GERD:

  • Coffee and alcohol stimulate gastric acid secretion. Taking these before bedtime especially can cause evening reflux.
  • Antacids based on calcium carbonate (but not aluminum hydroxide) were found to actually increase the acidity of the stomach. However, all antacids reduced acidity in the lower esophagus, so the net effect on GERD symptoms may still be positive.[17]
  • Foods high in fats and smoking reduce lower esophageal sphincter competence, so avoiding these may help. Fat also delays stomach emptying.
  • Eating within 2–3 hours before bedtime.
  • Large meals. Having smaller, more frequent meals reduces GERD risk, as it means there is less food in the stomach at any one time.
  • Carbonated soft drinks with or without sugar.
  • Chocolate and peppermint.
  • Acidic foods: tomatoes and tomato-based preparations; citrus fruits and citrus juices.
  • Cruciferous vegetables: cabbage, cauliflower, broccoli, and Brussels sprouts.
  • Milk and milk-based products containing calcium and fat, within 2 hours of bedtime.

Positional therapy

Sleeping on the left side has been shown to reduce nighttime reflux episodes in patients. [18]

A meta-analysis suggested that elevating the head of bed is an effective therapy, although this conclusion was only supported by nonrandomized studies. [16] The head of the bed can be elevated by plastic or wooden bed risers that support bed posts or legs, a therapeutic bed wedge pillow, or a wedge or an inflatable mattress lifter that fits in between mattress and box spring. The height of the elevation is critical and must be at least 6 to 8 inches (15 to 20 cm) to be at least minimally effective to prevent the backflow of gastric fluids. Some innerspring mattresses do not work well when inclined and may cause back pain; some prefer foam mattresses. Some practitioners use higher degrees of incline than provided by the commonly suggested 6 to 8 inches (15 to 20 cm) and claim greater success.

Medications

A number of drugs are approved to treat GERD, and are among the most-often-prescribed forms of medication in most Western countries.

  • Proton pump inhibitors (such as omeprazole, pantoprazole, lansoprazole, and rabeprazole) are the most effective in reducing gastric acid secretion. These drugs stop acid secretion at the source of acid production, i.e., the proton pump.
  • Gastric H2 receptor blockers (such as ranitidine, famotidine and cimetidine) can reduce gastric secretion of acid. These drugs are technically antihistamines. They relieve complaints in about 50% of all GERD patients. Compared to placebo (which also is associated with symptom improvement), they have a number needed to treat of eight (8).[19]
  • Antacids before meals or symptomatically after symptoms begin can reduce gastric acidity (increase pH).
  • Alginic acid (Gaviscon) may coat the mucosa as well as increase pH and decrease reflux. A meta-analysis of randomized controlled trials suggests alginic acid may be the most effective of non-prescription treatments with a number needed to treat of four.[19]
  • Prokinetics strengthen the lower esophageal sphincter (LES) and speed up gastric emptying. Cisapride, a member of this class, was withdrawn from the market for causing Long QT syndrome. Reglan (metoclopramide) is a prokinetic with significant side effects called Tardive Dyskinesia/Dystonia. [10] The United States Food and Drug Administration issued a Black Box Warning about Reglan in January 2009.
  • Sucralfate (Carafate) is also useful as an adjunct in helping to heal and prevent esophageal damage caused by GERD, however it must be taken several times daily and at least two (2) hours apart from meals and medications.
  • Mosapride citrate is a 5-HT4 receptor agonist used outside the United States largely as a therapy for GERD and dyspepsia.[20]

Supplement Support Approach

Aloe Vera Tablets and Deglycyrrhizinated Licorice

References:

1. DeVault KR, Castell DO (1999). “Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology”. Am. J. Gastroenterol. 94 (6): 1434–42. doi:10.1111/j.1572-0241.1999.1123_a.x. PMID 10364004.

2. “The saliva PH test and cancer“. Healingdaily.com. http://www.healingdaily.com/conditions/saliva-ph-test.htm. Retrieved 2009-08-19.

3. Kahrilas, PJ (2008). “Gastroesophageal Reflux Disease“. New England Journal of Medicine. 359 (16): 1700–1707. doi:10.1056/NEJMcp0804684. http://content.nejm.org/cgi/content/short/359/16/1700.

4. “Consumer Health Information“. Healthlink.mcw.edu. http://healthlink.mcw.edu/article/968784529.html. Retrieved 2009-08-19.

5. “Spitting Up in Babies“. familydoctor.org. http://familydoctor.org/online/famdocen/home/children/parents/infants/218.html.

6. Barrett’s Esophagus. Retrieved on 2009-02-01.

7. Diagnosis – Endoscopy. Retrieved on 2009-03-20.

8. Piesman M, Hwang I, Maydonovitch C, Wong RK (2007). “Nocturnal reflux episodes following the administration of a standardized meal. Does timing matter?”. Am. J. Gastroenterol. 102 (10): 2128–2134. doi:10.1111/j.1572-0241.2007.01348.x. PMID 17573791.

9. Ayazi S, Crookes P, Peyre C, (2007). “Objective documentation of the link between gastroesophageal reflux disease and obesity”. Am. J. Gastroenterol. 102 (S): 138–139.

10. Ayazi, Shahin; Chan, Linda S. (August 2009). “[http:// http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2710497&blobtype=pdf Obesity and gastroesophageal reflux: quantifying the association between body mass index, esophageal acid exposure, and lower esophageal sphincter status in a large series of patients with reflux symptoms]“. Journal of Gastrointestinal Surgery: 1440-7. http:// http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2710497&blobtype=pdf. Retrieved 2009-09-07.

11. Morse CA, Quan SF, Mays MZ, Green C, Stephen G, Fass R (2004). “Is there a relationship between obstructive sleep apnea and gastroesophageal reflux disease?”. Clin. Gastroenterol. Hepatol. 2 (9): 761–8. doi:10.1016/S1542-3565(04)00347-7. PMID 15354276.

12. Kasasbeh A, Kasasbeh E, Krishnaswamy G (2007). “Potential mechanisms connecting asthma, esophageal reflux, and obesity/sleep apnea complex—a hypothetical review”. Sleep Med Rev 11 (1): 47–58. doi:10.1016/j.smrv.2006.05.001. PMID 17198758.

13. H.J. O’Connor (Feb 1999). “Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management”. Aliment Pharmacol Ther 13 (2): 117-27. doi:10.1046/j.1365-2036.1999.00460.x. PMID 10102940.

14. El-Omar E, Oien K, Nujuni AE, et al. (1997). “Helicobacter pylori infection and chronic gastric acid hyposecretion”. Gastroenterology 113: 15–24 opt=Abstract. PMID 9207257.

15. C.A. Fallone, A.N. Barkun, S. Mayrand, G. Wakil, G. Friedman, A. Szilagyi, C. Wheeler & D. Ross (2004). “There is no difference in the disease severity of gastro-oesophageal reflux disease between patients infected and not infected with Helicobacter pylori“. Aliment Pharmacol Ther 20 (7): 761-768. doi:10.1111/j.1365-2036.2004.02171.x. http://www3.interscience.wiley.com/cgi-bin/fulltext/118774431/HTMLSTART.

16. Kaltenbach T, Crockett S, Gerson LB (2006). “Are lifestyle measures effective in patients with gastroesophageal reflux disease? An evidence-based approach”. Arch. Intern. Med. 166 (9): 965–71. doi:10.1001/archinte.166.9.965. PMID 16682569.

17. Decktor DL, Robinson M, Maton PN, Lanza FL, Gottlieb S (1995). “Effects of Aluminum/Magnesium Hydroxide and Calcium Carbonate on Esophageal and Gastric pH in Subjects with Heartburn”. Am J Ther 2 (8): 546–552. doi:10.1097/00045391-199508000-00006. PMID 11854825.

18. Khoury, RM; Camacho-Lobato L, Katz PO, Mohiuddin MA, Castell DO (1999). “Influence of spontaneous sleep positions on nighttime recumbent reflux in patients with gastroesophageal reflux disease”. Am. J. Gastroenterol. 94 (8): 2069–73. doi:10.1111/j.1572-0241.1999.01279.x. PMID 10445529.

19. Tran T, Lowry A, El-Serag H (2007). “Meta-analysis: the efficacy of over-the-counter gastro-oesophageal reflux disease drugs”. Aliment Pharmacol Ther 25 (2): 143–53. doi:10.1111/j.1365-2036.2006.03135.x. PMID 17229239.

15. Cash, B.D.; Chey, W.D.. “Role of Serotonergic Agents in Primary Chronic Constipation: Serotonergic Agents and Chronic Constipation“. MedScape. pp. 4. http://www.medscape.com/viewarticle/518324_4. Retrieved 2009-09-07.

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I Need to Better Understand My Attention-deficit Hyperactivity Disorder and Can Omega-3 Fatty Acid Supplements Help Me and My Family?

I need to better understand my Attention-deficit hyperactivity disorder (ADHD or AD/HD) and determine what I can do about it. Attention-deficit hyperactivity disorder is a neurobehavioral [1] developmental disorder.[2] ADHD is primarily characterized by “the co-existence of attention problems and hyperactivity, with each behavior occurring infrequently alone.”[3] While symptoms may appear to be innocent and merely annoying nuisances to observers, “if left untreated, the persistent and pervasive effects of ADHD symptoms can insidiously and severely interfere with one’s ability to get the most out of education, fulfill one’s potential in the workplace, establish and maintain interpersonal relationships, and maintain a generally positive sense of self.”[4]

ADHD is the most commonly studied and diagnosed psychiatric disorder in children, affecting about 3 to 5% of children globally with symptoms starting before seven years of age.[5][6] ADHD is a common chronic disorder in children[7] with 30 to 50% of those individuals diagnosed in childhood continuing to have symptoms into adulthood.[8][9] Adolescents and adults with ADHD tend to develop coping mechanisms to compensate for some or all of their impairments.[10] However, many aspects of daily life that most people take for granted are rendered more difficult by the symptoms of ADHD.[4]

Though previously regarded as a childhood diagnosis, ADHD can continue throughout adulthood.[11] 4.7 percent of American adults are estimated to live with ADHD.[12] ADHD is diagnosed two to four times as frequently in boys as in girls,[13][14] though studies suggest this discrepancy may be due to subjective bias of referring teachers.[15] ADHD management usually involves some combination of medications, behavior modifications, lifestyle changes, and counseling. Its symptoms can be difficult to differentiate from other psychiatric or other disorders, increasing the likelihood that the diagnosis of ADHD will be missed.[4] Additionally, most clinicians have not received formal training in the assessment and treatment of ADHD, particularly in adult patients.[4]

ADHD and its diagnosis and treatment have been considered controversial since the 1970s.[16] The controversies have involved clinicians, teachers, policymakers, parents and the media. Opinions regarding ADHD range from not believing it exist at all to believing there are genetic and physiological bases for the condition as well as disagreement about the use of stimulant medications in treatment.[17][18][19] Most healthcare providers accept that ADHD is a genuine disorder with debate in the scientific community centering mainly around how it is diagnosed and treated.[20][21][22] The AMA Council on Scientific Affairs concluded in 1998 that “diagnostic criteria for ADHD are based on extensive empirical research and, if applied appropriately, lead to the diagnosis of a syndrome with high reliability, good face validity, and high predictability of course and medication responsiveness.”[23]

ADHD may be seen as one or more continuous traits found normally throughout the general population.[24] ADHD is a developmental disorder in which certain traits such as impulse control lag in development.[25] Using magnetic resonance imaging of the prefrontal cortex, this developmental lag has been estimated to range from 3 to 5 years.[26] These delays are considered to cause impairment. ADHD has also been classified as a behavior disorder. [27] A diagnosis of ADHD does not, however, imply a neurological disease. [24]

ADHD is classified as a disruptive behavior disorder along with oppositional defiant disorder, conduct disorder and antisocial disorder.[28]

Subtypes

ADHD has three subtypes: [29]

  • Predominantly hyperactive-impulsive
    • Most symptoms (six or more) are in the hyperactivity-impulsivity categories.
    • Fewer than six symptoms of inattention are present, although inattention may still be present to some degree.
  • Predominantly inattentive
    • The majority of symptoms (six or more) are in the inattention category and fewer than six symptoms of hyperactivity-impulsivity are present, although hyperactivity-impulsivity may still be present to some degree.
    • Children with this subtype are less likely to act out or have difficulties getting along with other children. They may sit quietly, but they are not paying attention to what they are doing. Therefore, the child may be overlooked, and parents and teachers may not notice symptoms of ADHD.
  • Combined hyperactive-impulsive and inattentive
    • Six or more symptoms of inattention and six or more symptoms of hyperactivity-impulsivity are present.
    • Most children have the combined type of ADHD

Childhood ADHD

Attention-deficit hyperactivity disorder or ADHD is a common childhood illness that can be treated. It is a health condition involving biologically active substances in the brain. ADHD may affect certain areas of the brain that allow problem solving, planning ahead, understanding others’ actions, and impulse control.[30]

The American Academy of Child Adolescent Psychiatry (AACAP) considers it necessary that the following be present before attaching the label of ADHD to a child:

  • The behaviors must appear before age 7.
  • They must continue for at least six months.
  • The symptoms must also create a real handicap in at least two of the following areas of the child’s life:
    • in the classroom,
    • on the playground,
    • at home,
    • in the community, or
    • in social settings.[30]

If a child seems too active on the playground but not elsewhere, the problem might not be ADHD. It might also not be ADHD if the behaviors occur in the classroom but nowhere else. A child who shows some symptoms would not be diagnosed with ADHD if his or her schoolwork or friendships are not impaired by the behaviors.[30]

Even if a child’s behavior seems like ADHD, it might not actually be ADHD. Many other conditions and situations can trigger behavior that resembles ADHD. For example, a child might show ADHD symptoms when experiencing:

  • A death or divorce in the family, a parent’s job loss, or other sudden change
  • Undetected seizures
  • An ear infection that causes temporary hearing problems
  • Problems with schoolwork caused by a learning disability
  • Anxiety or depression[30]
  • Insufficient or poor quality sleep

Adult ADHD

It has been estimated that about eight million adults have ADHD in the United States.[31] Untreated adults with ADHD often have chaotic lifestyles, may appear to be disorganized and may rely on non-prescribed drugs and alcohol to get by.[32] They often have such associated psychiatric co morbidities as depression, anxiety disorder, bipolar disorder, substance abuse, or a learning disability.[32] A diagnosis of ADHD may offer adults insight into their behaviors and allow patients to become more aware and seek help with coping and treatment strategies.[31] There is controversy amongst some experts on whether ADHD persists into adulthood. Recognized as occurring in adults in 1978, it is currently not addressed separately from ADHD in childhood. Obstacles that clinicians face when assessing adults who may have ADHD include developmentally inappropriate diagnostic criteria, age-related changes, co morbidities and the possibility that high intelligence or situational factors can mask ADHD. [33]

Symptoms

Inattention, hyperactivity, and impulsivity are the key behaviors of ADHD. The symptoms of ADHD are especially difficult to define because it is hard to draw the line at where normal levels of inattention, hyperactivity, and impulsivity end and clinically significant levels requiring intervention begin. [4] In children with ADHD, these behaviors are more severe and occur more often. To be diagnosed with the disorder, a child must have symptoms for 6 or more months and to a degree that is greater than other children of the same age.

The symptom categories of ADHD in children yield three potential classifications of ADHD—predominantly inattentive type, predominantly hyperactive-impulsive type, or combined type if criteria for both subtypes are met: [4]

Predominantly inattentive type symptoms may include: [34]

  • Be easily distracted, miss details, forget things, and frequently switch from one activity to another
  • Have difficulty focusing on one thing
  • Become bored with a task after only a few minutes, unless they are doing something enjoyable
  • Have difficulty focusing attention on organizing and completing a task or learning something new
  • Have trouble completing or turning in homework assignments, often losing things (e.g., pencils, toys, assignments) needed to complete tasks or activities
  • Not seem to listen when spoken to
  • Daydream, become easily confused, and move slowly
  • Have difficulty processing information as quickly and accurately as others
  • Struggle to follow instructions.

Predominantly hyperactive-impulsive type symptoms may include: [34]

  • Fidget and squirm in their seats
  • Talk nonstop
  • Dash around, touching or playing with anything and everything in sight
  • Have trouble sitting still during dinner, school, and story time
  • Be constantly in motion
  • Have difficulty doing quiet tasks or activities.

and also these manifestations primarily of impulsivity:[34]

  • Be very impatient
  • Blurt out inappropriate comments, show their emotions without restraint, and act without regard for consequences
  • Have difficulty waiting for things they want or waiting their turns in games

Most people exhibit some of these behaviors, but not to the degree where such behaviors significantly interfere with a person’s work, relationships, or studies. The core impairments are consistent even in different cultural contexts. [35]

Symptoms may persist into adulthood for well over half of children diagnosed with ADHD. Estimating this is difficult as there are no official diagnostic criteria for ADHD in adults.[4]

A 2009 study found that children with ADHD move around a lot because it helps them stay alert enough to complete challenging tasks. [36]

ADHD and Co morbid Disorders

ADHD may accompany other disorders such as anxiety or depression. Such combinations can greatly complicate diagnosis and treatment. Academic studies and research in private practice suggest that depression in ADHD appears to be increasingly prevalent in children as they get older, with a higher rate of increase in girls than in boys, and to vary in prevalence with the subtype of ADHD. Where a mood disorder complicates ADHD it would be prudent to treat the mood disorder first, but parents of children who have ADHD often wish to have the ADHD treated first, because the response to treatment is quicker. [37]

Inattention and “hyperactive” behavior are not the only problems in children with ADHD. ADHD exists alone in only about 1/3 of the children diagnosed with it. Many co-existing conditions require other courses of treatment and should be diagnosed separately instead of being grouped in the ADHD diagnosis. Some of the associated conditions are:

  • Oppositional defiant disorder (35%) and conduct disorder (26%) which both are characterized by anti-social behaviors such as stubbornness, aggression, frequent temper tantrums, deceitfulness, lying, or stealing.[38]
  • Primary disorder of vigilance, which is characterized by poor attention and concentration, as well as difficulties staying awake. These children tend to fidget, yawn and stretch and appear to be hyperactive in order to remain alert and active.[38]
  • Mood disorders. Boys diagnosed with the combined subtype have been shown more likely to suffer from a mood disorder.[39]
  • Bipolar disorder. As many as 25% of children with ADHD have bipolar disorder. Children with this combination may demonstrate more aggression and behavioral problems than those with ADHD alone.[38]
  • Anxiety disorder, which has been found to be more common in girls diagnosed with the inattentive subtype of ADHD.[40]
  • Obsessive-compulsive disorder. OCD is believed to share a genetic component with ADHD and shares many of its characteristics.[38]

Causes

A specific cause of ADHD is not known. [41] There are, however, a number of factors that may contribute to ADHD including genetics, diet and social and physical environments.

Genetic factors

Twin studies indicate that the disorder is highly heritable and that genetics are a factor in about 75% of ADHD cases.[24] Hyperactivity also seems to be primarily a genetic condition; however, other causes do have an effect.[42]

Researchers believe that a large majority of ADHD cases arise from a combination of various genes, many of which affect dopamine transporters. Candidate genes include dopamine transporter, dopamine receptors D2/D3,[43] dopamine beta-hydroxylase monoamine oxidase A, catecholamine-methyl transferase, serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), 5-hydroxytryptamine 1B receptor (5-HT1B),[44] the 10-repeat allele of the DAT1 gene,[45] the 7-repeat allele of the DRD4 gene,[45] and the dopamine beta hydroxylase gene.[46]

The broad selection of targets indicates that ADHD does not follow the traditional model of a “genetic disease” and should therefore be viewed as a complex interaction among genetic and environmental factors. Even though all these genes might play a role, to date no single gene has been shown to make a major contribution to ADHD. [47]

Evolutionary theories

The hunter vs. farmer theory is a hypothesis proposed by author Thom Hartmann about the origins of ADHD. The theory proposes that hyperactivity may be an adaptive behavior in pre modern humans.[48] And that those with ADHD retain some of the older “hunter” characteristics associated with early pre-agricultural human society. According to this theory, individuals with ADHD may be more adept at searching and seeking and less adept at staying put and managing complex tasks over time. [49] Further evidence showing hyperactivity may be evolutionarily beneficial was put forth in 2006 in a study which found it may carry specific benefits for a society.[50]

Environmental factors

Twin studies to date have also suggested that approximately 9% to 20% of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be attributed to nonshared environmental (nongenetic) factors.[51][52]

Environmental factors implicated include alcohol and tobacco smoke exposure during pregnancy and environmental exposure to lead in very early life.[53] The relation of smoking to ADHD could be due to nicotine causing hypoxia (lack of oxygen) to the fetus in utero.[54] It could also be that women with ADHD are more likely to smoke[55] and therefore, due to the strong genetic component of ADHD, are more likely to have children with ADHD.[56] Complications during pregnancy and birth—including premature birth—might also play a role.[57] ADHD patients have been observed to have higher than average rates of head injuries;[58] however, current evidence does not indicate that head injuries are the cause of ADHD in the patients observed.[59]

Diet

A study[60] conducted by researchers at Southampton University in the United Kingdom and published in The Lancet on November 3, 2007 found a definitive link between children’s ingestion of many commonly used artificial food colors, the preservative sodium benzoate and hyperactivity. In response to these findings, the British government took prompt action. According to the Food Standards Agency, the food regulatory agency in the UK, food manufacturers are being encouraged to voluntarily phase out the use of most artificial food colors by the end of 2009. Following the FSA’s actions, the European Commission ruled that any food products containing the “Southampton Six” must display warning labels on their packaging by 2010. In the US, little has been done to curb food manufacturer’s use of artificial food colors, despite the new evidence presented by the Southampton study. However, the existing US Food Drug and Cosmetic Act [61] had already required that artificial food colors be approved for use, that they must be given FD&C numbers by the FDA, and the use of these colors must be indicated on the package[62]. This is why food packaging in the USA may state something to the effect of: “Contains FD&C Red #40.”

Social factors

There is no compelling evidence that social factors alone can cause ADHD.[25] However, many researchers believe that relationships with caregivers have a profound effect on attention and self-regulatory abilities. A study of foster children found that a high number of them had symptoms closely resembling ADHD,[63] while other researchers have found behavior typical of ADHD in children who have suffered violence and emotional abuse.[24][64] Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD.[65] ADHD is also considered to be related to sensory integration dysfunction.[66]

Neurodiversity

Proponents of this theory assert that atypical (neurodivergent) neurological development is a normal human difference that is to be tolerated and respected just like any other human difference. Social critics argue that while biological factors may play a large role in difficulties with sitting still in class and/or concentrating on schoolwork in some children, these children could have failed to integrate others’ social expectations of their behavior for a variety of other reasons.[67] Others have said that ADHD has a link with creativity.[68] As genetic research into ADHD proceeds, it may become possible to integrate this information with the neurobiology in order to distinguish disability from varieties of normal or even exceptional functioning in people along the same spectrum of attention differences.[69]

Pathophysiology

The pathophysiology of ADHD is unclear and there are a number of competing theories.[76] 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.[77] Neuroimaging studies in ADHD have not always given consistent results and as of 2008 are only used for research not diagnostic purposes.[78] 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.[79]

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.[80] It should be noted that stimulant medication itself may affect growth factors of the central nervous system.[81]

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. [82]

Additionally, SPECT scans found people with ADHD to have reduced blood circulation (indicating low neural activity),[83] and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead.[84][85] 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 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 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. [86]

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.[87] Further studies found that chronic stimulant treatment had little effect on global glucose metabolism,[88] 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. [89] 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.[90] 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.[91][92][93]

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[94] 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. [95][96] They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.[95]

Diagnosis

ADHD is diagnosed via a psychological assessment; to rule out other potential causes or comorbidities, physical examination, radiological imaging, and laboratory tests may be used. [97]

In North America, the DSM-IV criteria are often the basis for a diagnosis, while European countries usually use the ICD-10.[98] If the DSM-IV criteria is used rather than the ICD-10 a diagnosis ADHD is 3–4 times more likely.[14] Factors other than those within the DSM or ICD however have been found to effect the diagnosis in clinical practice. A child’s social and school environments as well as academic pressures at school are likely to be of influence. [99]

Many of the symptoms of ADHD occur from time to time in everyone; in patients with ADHD, the frequency of these symptoms is greater and patients’ lives are significantly impaired. Impairment must occur in multiple settings to be classified as ADHD. As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these criteria are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

  1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
  2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
  3. ADHD, Predominantly Hyperactive-Impulsive Type: if criterion 1B is met but criterion 1A is not met for the past six months.

The previously used term ADD expired with the most recent revision of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

Pharmacological treatment

Management with medication has been shown to be the most cost-effective, followed by behavioral treatment and combined treatment in a 14 month follow-up study.[100] However, a longer follow-up study of 3 years found that stimulant medication offered no benefits over behavioral therapy.[101] 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.[102] The long term effects of ADHD medications in preschool children are unknown and are not recommended for pre-school children.[24][103] There is very little data on the long-term adverse effects or benefits of stimulants for ADHD.[104]

Supplement Support Approach

Dietary supplements and specialized diets are sometimes used by people with ADHD with the intent to mitigate some or all of the symptoms. For example, Omega-3 supplementation may reduce ADHD symptoms for a subgroup of children and adolescents with ADHD “characterized by inattention and associated neurodevelopmental disorders.”[105] Although vitamin or mineral supplements (micronutrients) may help children diagnosed with particular deficiencies, there is no evidence that they are helpful for all children with ADHD. Furthermore, mega doses of vitamins, which can be toxic, must be avoided.[106]

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  88. Matochik JA, Liebenauer LL, King AC, Szymanski HV, Cohen RM, Zametkin AJ (May 1994). “Cerebral glucose metabolism in adults with attention deficit hyperactivity disorder after chronic stimulant treatment“. Am J Psychiatry 151 (5): 658–64. PMID 8166305. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=8166305.
  89. Zametkin AJ, Liebenauer LL, Fitzgerald GA, et al. (May 1993). “Brain metabolism in teenagers with attention-deficit hyperactivity disorder”. Arch. Gen. Psychiatry 50 (5): 333–40. PMID 8489322.
  90. Ernst M, Cohen RM, Liebenauer LL, Jons PH, Zametkin AJ (October 1997). “Cerebral glucose metabolism in adolescent girls with attention-deficit/hyperactivity disorder”. J Am Acad Child Adolesc Psychiatry 36 (10): 1399–406. doi:10.1097/00004583-199710000-00022. PMID 9334553.
  91. Armstrong, Thomas (1999). MAVM2K6SdAfcSf0nGYQ&hl=en&sa=X&oi=book_result&resnum=1&ct=result#PPA3,M1 Add/Adhd Alternatives in the Classroom. ASCD. pp. 3–5. ISBN 9780871203595. http://books.google.ca/books?id=EzXt100I4A8C&pg=PA3&lpg=PA3&dq=National+Institute+of+Mental+Health+ADHD+PET+scan&source=web&ots=GlP-TIeiqN&sig=JADzxFyez- MAVM2K6SdAfcSf0nGYQ&hl=en&sa=X&oi=book_result&resnum=1&ct=result#PPA3,M1. Retrieved 2009-05-02.
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Anxiety and Feelings of Dying

Anxiety is a psychological and physiological state characterized by cognitive, somatic, emotional, and behavioral components. [1] These components combine to create an unpleasant feeling that is typically associated with uneasiness, fear, or worry.

Anxiety is a generalized mood condition that occurs without an identifiable triggering stimulus. As such, it is distinguished from fear, which occurs in the presence of an observed threat. Additionally, fear is related to the specific behaviors of escape and avoidance, whereas anxiety is the result of threats that are perceived to be uncontrollable or unavoidable. [2]

Another view is that anxiety is “a future-oriented mood state in which one is ready or prepared to attempt to cope with upcoming negative events”[3] suggesting that it is a distinction between future vs. present dangers that divides anxiety and fear.

Anxiety is considered to be a normal reaction to stress. It may help a person to deal with a difficult situation, for example at work or at school, by prompting one to cope with it. When anxiety becomes excessive, it may fall under the classification of an anxiety disorder. [4]

Diagnosis

Anxiety disorders are often debilitating chronic conditions, which can be present from an early age or begin suddenly after a triggering event. They are prone to flare up at times of high stress and are frequently accompanied by physiological symptoms such as headache, sweating, muscle spasms, palpitations, and hypertension, which in some cases lead to fatigue or even exhaustion.

Although in casual discourse the words anxiety and fear are often used interchangeably, in clinical usage, they have distinct meanings; anxiety is defined as an unpleasant emotional state for which the cause is either not readily identified or perceived to be uncontrollable or unavoidable, whereas fear is an emotional and physiological response to a recognized external threat. The term anxiety disorder, however, includes fears as well as anxieties. Indeed, phobias (fears which are “persistent or irrational”) constitute the majority of anxiety disorder cases.

Anxiety disorders are often co morbid with other mental disorders, particularly clinical depression, which may occur in as many as 60% of people with anxiety disorders. The fact that there is considerable overlap between symptoms of anxiety and depression, and that the same environmental triggers can provoke symptoms in either condition, may help to explain this high rate of comorbidity. [3]

Studies have also indicated that anxiety disorders are more likely among those with family history of anxiety disorders, especially certain types.[4]

Sexual dysfunction also often accompanies anxiety disorders, although it is difficult to determine whether anxiety causes the sexual dysfunction, or whether they arise from a common cause. The most common manifestations in individuals with anxiety disorder are avoidance of intercourse, premature ejaculation or erectile dysfunction among men and pain during intercourse among women. Sexual dysfunction is particularly common among people affected by panic disorder (who may fear that a panic attack will occur during sexual arousal) and posttraumatic stress disorder. [5]

Treatment

Treatment options available include lifestyle changes; psychotherapy, especially cognitive behavioral therapy; and pharmaceutical therapy. Education, reassurance and some form of cognitive-behavioral therapy should almost always be used in treatment.

When medication is indicated SSRIs, such as fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil) and escitalopram (Lexapro) are generally recommended as first line agents. SNRIs such as venlafaxine (Effexor) are also effective. Benzodiazepines, such as alprazolam (Xanax), clonazepam (Klonopin) and diazepam (Valium) are also sometimes indicated for short-term or PRN use. They are usually considered as a second line treatment due to disadvantages such as cognitive impairment and due to their risks of dependence and withdrawal problems.[9] Other medications commonly prescribed for anxiety disorders include GABA analogues such as gabapentin (Neurontin) or pregabalin (Lyrica), MAOIs such as phenelzine (Nardil) or tranylcypromine (Parnate), as well as the novel antidepressant mirtazapine (Remeron). TCAs such as imipramine, as well as atypical antipsychotics such as quetiapine, and piperazines such as hydroxyzine are also occasionally prescribed.[10]

Treatment controversy arises because while some studies indicate that a combination of medication and psychotherapy can be more effective than either one alone; others suggest pharmacological interventions are largely palliative, and can actually interfere with the mechanisms of successful therapy.[11] Meta-analysis indicates that psychotherapeutic interventions have superior long-term efficacy when compared to pharmacotherapy.[12] However, the right treatment may very much depend on the individual patient’s genetics and environmental factors.

Regular aerobic exercise, improving sleep hygiene and reducing caffeine are often useful in treating anxiety.

Supplement Support Approach

Low levels of GABA( gamma-aminobutyric acid), a neurotransmitter that reduces activity in the central nervous system, contribute to anxiety. A number of anxiolytics achieve their effect by modulating the GABA receptors. [5][6][7]

Acetyl-L-Carnitine, Ashwaganda, Dimethylaminoethanol, Ginkgo Biloba, L-Glutamine, L-Pyroglutamine Acid, L-Tyrosine, and Phosphatidyl Complex has shown support in times of dietary support needs. [8]

Caution Advised when taking the following supplements with anxiety disorder:

Guaraná may lead to possible cardiovascular side effects. Cardiovascular disease refers to the class of diseases that involve the heart and/or blood vessels (arteries and veins). While the term technically refers to any disease that affects the cardiovascular system, it is usually used to refer to those related to atherosclerosis (arterial disease).

Kola Nut may increase risk of caffeine induced adverse effects and possibly inhibit liver metabolism. Caffeine is a xanthenes alkaloid compound that acts as a stimulant in humans.

References:

1. Seligman, M.E.P., Walker, E.F. & Rosenhan, D.L. (2001). Abnormal psychology, (4th ed.) New York: W.W. Norton & Company, Inc.

2. Ohman, A. (2000). Fear and anxiety: Evolutionary, cognitive, and clinical perspectives. In M. Lewis & J. M. Haviland-Jones (Eds.). Handbook of emotions. (pp.573-593). New York: The Guilford Press.

3. ^ Barlow, David H. (November 2002). “Unraveling the mysteries of anxiety and its disorders from the perspective of emotion theory“. American Psychologist: 1247-63. http://psycnet.apa.org/journals/amp/55/11/1247.pdf.

4. National Institute of Mental Health Retrie.ved September 3, 2008.

5. “The role of GABA in anxiety disorders.”. J Clin Psychiatry 64 (Suppl 3): 21–7. 2003. PMID : 12662130.

6. “The role of GABA in the pathophysiology and treatment of anxiety disorders.”. Psychopharmacol Bull 37 (4): 133–46. 2003. PMID : 15131523.

7. “Role of gamma-aminobutyric acid in anxiety.”. Psychopathology.;: 17 (Suppl 1): 15–24. 1984. PMID: 6143341.

8. Egrets Data Base, 2009.

9. Stein, Dan J (16 February 2004). Clinical Manual of Anxiety Disorders (1st ed.). USA: American Psychiatric Press Inc. p. 7. ISBN 978-1585620760. http://books.google.co.uk/books?id=44reFIgFDBMC.

10. Llorca PM, Spadone C, Sol O, et al. (November 2002). “Efficacy and safety of hydroxyzine in the treatment of generalized anxiety disorder: a 3-month double-blind study“. J Clin Psychiatry 63 (11): 1020–7. PMID 12444816. http://www.psychiatrist.com/privatepdf/2002/v63n11/v63n1112.pdf.

11. Hollon S; Stewart O, Strunk D (August 25, 2005). “Enduring effects for Cognitive Behavior Therapy in the Treatment of Depression and Anxiety” (PDF). Annual Review of Psychology 57: 285–315. doi:10.1146/annurev.psych.57.102904.190044. http://faculty.psy.ohio-state.edu/strunk/personal/Hollon,%20Stewart,%20&%20Strunk%20enduring%20effects%20AR%202006.pdf.

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