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Culture Specific Syndrome

Culture Specific Syndrome.
ultural Bound Syndromes Culture-bound syndrome The term culture-bound syndrome was included in the fourth version of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2000) which also includes a list of the most common culture-bound conditions (DSM-IV: Appendix I). Included in DSM-IV-TR (4th. ed) the term cultural-bound syndrome denotes recurrent, locality-specific patterns of abnormal behavior and troubling experience that may or may not be linked to a particular DSM-IV-TR diagnostic category.
Many of these patterns are naturally considered to be illnesses, or at least afflictions, and most have local names. Although presentations conforming to the major DSM-IV-TR categories can be found throughout the world, the particular symptoms, course, and social response are very often influenced by local cultural factors. In contrast, cultural-bound syndromes are generally limited to specific societies or culture areas and are localized, folk, diagnostic categories that frame coherent meanings for certain repetitive, patterned, and troubling sets of experiences and observations.
In medicine, a culture-specific syndrome or culture-bound syndrome is a combination of psychiatric and somatic symptoms that are considered to be a recognizable disease only within a specific society or culture. There are no objective biochemical or structural alterations of body organs or functions, and the disease is not recognized in other cultures. While a substantial portion of mental disorders, in the way they are manifested and experienced, are at least partially conditioned by the culture in which they are found, some disorders are more culture-specific than others.

The concept of culture-bound syndromes is very controversial and many psychologists, medical doctors, and anthropologists reject the concept. The identification of culture-specific syndromes: A culture-specific syndrome is characterized by: categorization as a disease in the culture (i. e. , not a voluntary behavior or false claim); widespread familiarity in the culture; complete lack of familiarity of the condition to people in other cultures; no objectively demonstrable biochemical or tissue abnormalities (symptoms); the condition is usually recognized and treated by the folk medicine of the culture.
Some culture-specific syndromes involve somatic symptoms (pain or disturbed function of a body part), while others are purely behavioral. Some culture-bound syndromes appear with similar features in several cultures, but with locally-specific traits, such as penis panics. A culture-specific syndrome is not the same as a geographically localized disease with specific, identifiable, causal tissue abnormalities, such as kuru or sleeping sickness, or genetic conditions limited to certain populations.
It is possible that a condition originally assumed to be a culture-bound behavioral syndrome is found to have a biological cause; from a medical perspective it would then be redefined into another nosological category. Western medical perspectives: An interesting aspect of culture-specific syndromes is the extent to which they are “real”. Characterizing them as “imaginary” is as inaccurate as characterizing them as “malingering”, but there is no clear way to understand them from a Western scientific perspective.
Culture-specific syndromes shed light on how our mind decides that symptoms are connected and how a society defines a known “disease”. In contrast, culture-bound syndromes are generally limited to specific societies or culture areas and are localized, folk, diagnostic [comma sic] categories that frame coherent meanings for certain repetitive, patterned, and troubling sets of experiences and observations.
Medical care of the condition is challenging and illustrates a truly fundamental but rarely discussed aspect of the physician-patient relationship: the need to negotiate a diagnosis that fits the way of looking at the body and its diseases of both parties. The physician may do any of the following: Share the way the patient sees the disorder, and offer the folk medicine treatment, recognize it as a culture-bound syndrome, but pretend to share the patient’s perspectives and offer the folk medicine reatment or a new improvised treatment, recognize it as a culture-bound syndrome but try to educate the patient into seeing the condition as the physician sees it. The problem with the first choice is that physicians who pride themselves on their knowledge of disease like to think they know the difference between culture-specific disorders and “organic” diseases. While the second choice may be the quickest and most comfortable choice, the physician must deliberately deceive the patient.
Currently in Western culture this is considered one of the most unethical things a physician can do, whereas in other times and cultures deception with benevolent intent has been an accepted tool of treatment. The third choice is the most difficult and time-consuming to do without leaving the patient disappointed, insulted, or lacking confidence in the physician, and may leave both physician and patient haunted by doubts (“Maybe the condition is real. ” or “Maybe this doctor doesn’t know what s/he is talking about. ”).
Root-work/Obeah: DSM IV-TR (2000), states that a set of cultural interpretations that ascribe illness to hexing, witchcraft, sorcery, or the evil influence of another person. Symptoms may include generalized anxiety and gastrointestinal complaints (e. g. , nausea, vomiting, and diarrhea), weakness, dizziness, the fear of being poisoned, and sometimes fear of being killed (voodoo death). DSM IV-TR site roots, spells, or hexes can be put or placed on other persons, causing a variety of emotional and psychological problems.
The hexed person may even fear death until the root has been taken off, or eliminated usually through the work of the root doctor (a healer in this tradition), who can also be called on to bewitch an enemy. Roots is found in the southern United States among both African-American and European American populations and in the Caribbean societies. Obeah (sometimes spelled “Obi”) is a term used in the West Indies to refer to folk magic, sorcery, and religious practices derived from Central African and West African origins. Obeah can either be a form of ‘dark’ magic or ‘good’ magic.
As such, Obeah is similar to Palo, Voodoo, Santeria, root-work, and hoodoo. Obeah (another name used in the Caribbean society) is practiced in Suriname, Jamaica, Haiti, the Virgin Islands, Trinidad and Tobago, Guyana, and Belize, the Bahamas, St. Vincent and the Grenadines, Barbados and many other Caribbean countries. Obeah is associated with both benign and malign magic, charms, luck, and with mysticism in general. In some Caribbean nations Obeah refers to African diasporic folk religions; in other areas, Christians may include elements of Obeah in their religion.
Obeah is often associated with the Spiritual Baptist church. Origins: In Jamaica, slaves from different areas of Africa were brought into contact, creating some conflicts between those who practiced varying African religions. Those of West African Ashanti descent, who called their priests “Myal men” (also spelled Mial men), used the Ashanti term “Obi” or “Obeah” — meaning “sorcery” — to describe the practices of slaves of Central African descent. Thus those who worked in a Congo form of folk religion were called “Obeah men” or “sorcerers. Obeah also came to mean any physical object, such as a talisman or charm that was used for evil magical purposes. However, despite its fearsome reputation, Obeah, like any other form of folk religion and folk magic, contains many traditions for healing, helping, and bringing about luck in love and money. Elements (key features/symptoms) According to Hughes, Simons &Wintrob, 1997 study, knowledge about a culture-bound syndrome, can address the relationship between the culture-bound syndrome and the more familiar psychiatric disorders, such as those in DSM-IV.
These researchers call this the comorbidity question on the assumption that studying the culture-bound syndrome’s patterned relationship to psychiatric diagnoses is a more fruitful approach than attempting prematurely to subsume it into the DSM diagnostic categories. Systematic research has identified strong correlations between culture-bound syndromes and criteria for psychiatric disorder, but there is rarely a one-to-one relationship between culture-bound syndrome and psychiatric disorder. The culture-bound syndromes often coexist with a range of psychiatric disorders, as many psychiatric disorders do with each other.
The comorbidity question brings culture-bound syndrome research in line with current approaches in psychiatric research. Differences in the symptomatic, emotional, and contextual aspects of cultural syndromes, in turn, may signal different comorbid relationships with psychiatric diagnosis or even the lack of such a relationship. Opinion The extra ordinary addition of culture-bound syndromes in DSM-IV provides the opportunity for improving the need to study such syndromes and the chance for developing a research to study them.
The growing ethnic and cultural diversity of the U. S. population presents a challenge to the mental health field to develop truly cross-cultural approaches to mental health research and services. This addition will give researchers the chance to study the relationship between culture-bound syndromes and psychiatric diagnoses. In my opinion a research program based on key questions is still unanswered, which is understanding culture-bound syndromes within their cultural context and to analyze the relationship between these syndromes and psychiatric disorders.
Reference DSM -IV-TR Diagnostic and Statistical Manual of Mental Disorders (2000). Publication manual of the American Psychological Association (4th ed. ). Washington, DC: Author. Hughes CC, Simons RC, Wintrob RM: The “Culture-Bound Syndromes” and DSM-IV, in DSM-IV Sourcebook, vol 3. Edited by Widiger TA, Frances AJ, Pincus HA, Ross R, First MB, Davis W. Washington, DC, American Psychiatric Association, 1997, pp 991–1000 Retrieved July 29, 2009 from American Journal of Psychiatry.

Culture Specific Syndrome

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Diabetes Mellitus Syndrome Chronic Hyperglycemia Health And Social Care Essay

Diabetes Mellitus Syndrome Chronic Hyperglycemia Health And Social Care Essay.

Diabetess mellitus was described more than 2000 old ages ago, one time regarded as a individual entity disease impacting persons of higher socio economic strata but now even the person of lower economic strata are besides affected. It is a disease characterized by a province of hyperglycaemia ensuing from diversenesss of etiologies, environmental and familial playing jointly.
By definition, diabetes mellitus is a syndrome characterized by chronic hyperglycaemia and perturbation of saccharides, protein and fat metamorphosis associated with absolute or comparative lack in insulin secernment and action.
Harmonizing to WHO, there are two chief types of diabetes mellitus ie insulin dependant diabetes mellitus ( type I ) and non insulin dependant diabetes mellitus ( type II ) .

Type II diabetes mellitus is a syndrome holding heterogenous and is associated with hazard of figure of complication like neurological, cardiovascular, nephritic, optic and musculoskeletal jobs. Out of these neurological and cardiovascular systems are normally affected.
Diabetess is systemic upset of energy metamorphosis in which hyperglycaemia is the cellular opposition to the consequence of insulin or both. Diabetes affects both the cardinal and peripheral nervous system.
Diabetic neuropathies are a household of nervus upset caused by diabetes. Peoples with diabetes can develop nervus harm throughout the organic structure. About 60 to 70 per centum of people with diabetes have some signifier of neuropathy. Peoples with diabetes can develop nerve jobs at any clip, but hazard rises with age and longer continuance of diabetes for more than 5 old ages. They appear to be more common in people who have jobs commanding their blood glucose besides called blood sugar.
Type II diabetes is the most common signifier of diabetes and normally appears in center aged grownups. Approximately 60-70 % of type II persons develop diabetic neuropathy. It is frequently associated with fleshiness and may be delayed or controlled with diet and exercising. Diabetic neuropathy appears to be more common in people over 45 – 55 old ages of age.
Causes: – Prolonged exposure to high blood sugar ( glucose ) can damage delicate nervus fibres, doing diabetic neuropathy. High blood glucose interferes with the ability of the nervousnesss to convey signals. It besides weakens the walls of the little blood vass that supply the nervousnesss with O and foods.
Metabolic factors, such as high blood glucose, long continuance of diabetes and perchance low degrees of insulin.
Neurovascular factors, taking to damage to the blood vass that carry O and foods to nervousnesss.
Autoimmune factors that cause redness in nervousnesss.
Clinical characteristics: –
Functional instability
Deep hurting most normally in the pess and legs
Numbness
Muscle failing
Loss of sense of warm or cold
Based on this Clinical characteristic that is functional instability, capable were evaluated with berg balance graduated table, incorporating 14 balance undertakings. Balance preparation to be an effectual agencies of forestalling falls in patients with diabetic neuropathy.
1.1 STATEMENT OF THE PROBLEM
This is a survey on the effectivity of balance exercising in bettering balance in patients with diabetic neuropathy.
1.2 AIMS AND OBJECTIVES OF THE STUDY
To happen out the effectivity of balance exercising in diabetic neuropathy patients
1.3 NEED AND SIGNIFICANCE OF THE STUDY
Diabetic neuropathy or nervus harm is a reasonably common diabetes related complication, approximately 60 % of individuals with diabetes have some grade of neuropathy and it is portion of regular tests and showings in individuals with diabetes about all individuals with diabetes will finally hold some signifier of neuropathy. Complication from neuropathy can run from mild to severe symptoms can include buzzing, firing or prickling paraesthesia in the pess and increased hazard of falling.
In this survey Berg balance graduated table was used to mensurate balance by measuring the public presentation of functional undertakings. This survey measure the effectivity of balance exercising to better balance in patients with diabetic neuropathy.
1.4 HYPOTHESIS
NULL HYPOTHESIS
There is no important difference in giving balance exercising to diabetic neuropathy patient.
ALTERNATIVE HYPOTHESIS
There is important difference in giving balance exercising to diabetic neuropathic patient.
1.5 OPERATIONAL DEFINITIONS
DIABETIC NEUROPATHY:
Diabetic neuropathies are a household of nervus upsets that are associated with diabetes mellitus. These conditions are thought to ensue from diabetic micro vascular hurt affecting little blood vass that supply nervousnesss.
Neuropathy is a nervus upset that consequences in deformation of nervus map.
TYPE II DIABETES:
Diabetess mellitus type II once called non insulin dependant diabetes mellitus or grownup oncoming diabetes is a upset that is characterized by high blood glucose in the context of insulin opposition and comparative insulin lack.
It is a chronic disease characterized by high degrees of sugar in the blood. It develops when your organic structure does non react right to insulin.
Balances:
The ability to aline organic structure sections against gravitation to keep or travel the organic structure ( centre of mass ) within the available base of support without falling.
2.REVIEW OF LITERATURE
a ) Reappraisal of literature related to diabetic neuropathy
RENUKA DHARMADHIKARI ( 2007 )
Mellitus is a common disease in people with about 50 % of type 2 diabetic patients being over 45 to 55 old ages of age. Insulin opposition is common in people, with big Numberss besides have impaired insulin secernment. Exercise with a peculiar accent on balance and stableness is an of import constituent of the direction and intervention of diabetic neuropathy patients.
D. FEEDLE, G. CUCINOTTA, DA GREENE ( 2005 )
A common complication of diabetics called neuropathy was determined in diabetic patients recruited from 109 out diabetic clinics. An increased consciousness of the high prevalence of neuropathy can take to early curative intercession and possible bar of ulterior neuropathic complication such as infection and pes ulcer.
ALI CIMBIZ, OZGE ( 2004 )
Diabetic neuropathy disturbed particularly the balance on the dominant leg. Done with 60 voluntary grownups of both sexes from Kuhatya, Turkey were divided in to two groups. A type 2 diabetic neuropathic group ( DG ) and a non diabetic control group ( CG ) . The CG was selected to fit the diabetic features such as age, organic structure mass and sex. Standing on dominant, non dominant leg and functional range were used for the appraisal.
STEFANO BALDUCCIAN, GIAN LUCA, LEOLCA PARISIC ( 2004 )
Exercise preparation can modify the natural history of diabetic neuropathy. This survey suggests for the first clip that long clip exercising preparation can forestall the oncoming or modify the natural history of diabetic neuropathy.
MARK J BROWN, JOHN R. MARTIN, ARTHUR K, ASBURY ( 1996 )
Diabetic patients whose neuropathy was characterized by hurting and autonomic disfunction with loss of balance and saving of musculus stretch physiological reactions.
YASUDA H DYCK P ( 1987 )
Hypothesized that neuropathy consequences from diseased developments in the little vass in diabetes by the observation of thickener of the walls of endoneurial capillaries in the nervus of diabetic patients as a consequence of an accretion of periodic Acid Schiff.
B ) Reappraisal of literature related to balance and diabetic neuropathy
ANN V. SCHWARTZ AND TERESA A. HILLIER ( 2001 )
Peoples with diabetic had increased hazard of falling in their survey conducted in patients with diabetic neuropathy. Postural stableness is the of import factor to keep the balance which reduces the hazard of autumn. Diabetic neuropathy topics may lose their Centre of force per unit area information for commanding postural sway in stance stage of pace.
HORAK FBB, DICKSTERIN R AND PETERCA R.J. ( 1998 )
Concluded that diabetic patients with neuropathy show higher scope and root mean square value compared with those of control topics and diabetic patients with out neuropathy quiet standing balance was investigated in 24 diabetic patients with or with out neuropathy with eyes opened and eyes closed.
DANIK LAFOND, HELENE CORIVEA AND FRANCIOS PRINCE ( 1998 )
Motor schemes at the mortise joint articulation are altered in diabetic neuropathy patients in his work subjected for postural control mechanism during quiet standing in patients with diabetic neuropathy.
BEVERLEIGH H PIEPERSA ( 1996 )
Many as one in two people with type 2 diabetes finally develops a status of chronic nervus harm in their pess known as diabetic neuropathy. Diabetic are at greater hazards for falls when they have fewer centripetal inputs to counterbalance for the loss of experiencing in their pess. Closing your eyes, or walking a across a dark room will ensue in more falls. Even standing on one pes is harder for a diabetic to make with their eyes closed, but easier if eyes are unfastened.
TABASSOM GHANAVATI, ALI ASGHAR ARASTOO: ( 1995 )
Diabetic neuropathy patients seems to do postural instability which may impact quality of maps and activities of day-to-day life of these patients.
ROTHWELL ( 1994 )
Ocular vestibular and proprioceptive subsystem response to somewhat different perturbation in balance. The visuo spinal system controls both inactive and faster inputs with proprioceptive system which is besides Sensitive to faster stimulation.
LORD ET.AL ( 1994 )
A survey in Australia reported that hapless balance is a factor in the causal tract between diabetes and increase hazard of falling. Thus the persons with diabetes had increased organic structure sway.
degree Celsius ) Review of literature related to consequence of exercising programme on balance upset
EMILY SPLICHAL: ( 1996 )
Diabetic neuropathy causes loss of distal strength and esthesis. Research has shown that diabetics with neuropathy are 15 times more likely to describe falling or faltering in a one twelvemonth period. Research has proven balance preparation to be an effectual agencies of forestalling falls in patient with diabetic neuropathy. All balance exercising can be done in a patient place with small or no equipment.
RICHARDSON J.K, SANDMAN D, VELA S.A ( 1995 )
Focused exercising regimen improves Clinical steps of balance in patients with diabetic neuropathy. Participants are 20 topics with diabetes mellitus and diagnostically confirmed patient. Ten subjects underwent a 3 hebdomad intercession exercising regimen designed to increase quickly available distal strength and balance. The other 10 topics performed a control exercising regimen. The intercession topics but non the control subjects, showed important betterment in all 3 clinical steps of balance that is impedal stance clip, Functional range and tandem stance clip.
vitamin D ) Review of literature related to berg balance graduated table
TRINA SMITH ( 2005 )
Berg Balance Scale used to quantify the balance of patients with diabetic neuropathy. Twenty one female and five males were selected. Participants completed each balance trial one time during 2 testing Sessionss for that inter rates dependability was good for the BBS. The balance trial showed moderate to good dependability for this population. The BBS appear to be valid steps of motor ability to keep balance.
GATEV ( 1999 )
Balance trials have been developed and presented to obtain appropriate information of balance measuring. The choice of mensurating clip and stance conditions is indispensable
ALEXANDER ( 1996 )
Balance trial have been developed and presented to obtain appropriate information of balance capablenesss during standing. Functional balance graduated tables are easy to execute and suitable for daily clinical usage that give more elaborate information about balance.
BEIG ETAL ( 1995 )
Berg Balance Scale in patients with damage of balance. It is a staff completed assessment graduated table of ability to keep balance either statistically or while executing assorted functional motions to assist do determinations about the patients equilibrate degree, comprises 14 discernible undertakings common to every twenty-four hours life.
3. RESEARCH DESIGN AND METHODOLOGY
3.1 REASEARCH DESIGN
This survey belongs to experimental design.
3.2 Variables USED IN THE STUDY
3.2.1 Independent variables
Balance exercising
Medical intervention
3.2.2 Dependent variable
Balance
3.3 Setting OF THE STUDY:
Physiotherapy Rehabilitation Centre, Kannur
3.4 CRITERIA FOR SELECTION
Inclusion standards
Diabetess with a continuance of more than 5 old ages
Type 2 diabetes with diagnosed neuropathy
Persons between the age group of 45-55 old ages were selected.
Both males and females wee included in this survey.
Patients who reported atleast one autumn in the past 6 months
Exclusion standards
Lower appendage amputation
Patients with inability to walk without any assistive devices
Patients with musculoskeletal damage
Patients with neurological damage
Diabetess with any other systemic engagement
3.5 SAMPLE POPULATION
30 Capable and 15 in each group
3.6 METHOD OF SAMPLING
Random Sampling Technique.
3.7 METHODOLOGY
30 Subjects are selected and divided in to two groups
The process was explained to subject.
GROUP A: Balance exercising with medical intervention
GROUP B: Medical intervention
3.8 Materials USED
Ruler
Two standard chairs ( one with a arm rests, one without )
Foot stool
Stop ticker or carpus ticker
Berg balance graduated table
Outcome measuring by utilizing Berg Balance graduated table
3.9 DURATION OF THE STUDY:
Four hebdomads
3.10 Procedure
The topics were given balance exercising like inactive and dynamic exercising for five yearss for four hebdomads. Entire intervention clip was 60 proceedingss /session/ twenty-four hours with 5 minute remainder after every 15 proceedingss.
Balance exercising
Improve balance by executing simple balance exercising. The individual leg stance is a really effectual exercising for bettering balance. This exercising can be modified balance stableness. The exercisings are categorized in to two different types inactive and dynamic of balance preparation.
Inactive exercising
Toe base
Tandum base
One – legged base
Heel base
Dynamic exercising in walking
Toe walk
Tandum forward walk
Heel walk
Tandum backward walk
1. Toe base
• Stand about one and a half pess off from the counter.
• Raise up every bit high as possible on the balls of your pess. Your pess should be shoulder width apart.
• Try to remain every bit still as possible. Make non travel your pess around to keep balance.
• Hold the toe base for 10 seconds.
Rest. Repeat 5 times.
2. Tandem Stand
• Stand about one and a half pess off from the counter.
• Place one pes straight in forepart of the other pes so that the heel of one pes is merely touching the toes of the other pes.
• Try to remain every bit still as possible. Make non travel your pess around to keep balance.
• Hold the tandem base for 10 seconds. Rest. Repeat 5 times.
3. One-legged Base
Stand about one and a half pess off from the counter.
Slowly lift one leg off of the floor, while keeping your balance with the other leg.
Try to remain every bit still as possible. Make non travel your pes around to keep balance.
Keep the one-legged base for 10 seconds.
Rest. Repeat with other leg 5 times.
4. Heel Stand
Stand about one and a half pess off from the counter.
Raise up every bit high as possible on the heels of your pess. Your pess should be shoulder width apart.
Try to remain every bit still as possible. Make non travel your pess around to keep balance.
Keep the heel base for 10 seconds.
Rest. Repeat 5 times.
Dynamic exercising
1. Toe walk
i»? • Go to one terminal of a hall and easy raise up every bit high as you can onto your toes. Walk down the hall on your toes.
• When you reach the other side, come down onto your pess and stand usually.
• Rest. Repeat 5 times.
2. i»? Tandem Forward Walk
Travel to one terminal of a hall and topographic point one pes in forepart of the other so that the heel of one pes touches the toes of the other pes.
Walk down the hall in a tandem walk.
It is of import that with each measure the heel of one pes touches the toes of the other. If you make a error, merely topographic point one pes in forepart of the other and go on down the hall.
When you reach the other side stand usually.
Rest. Repeat 5 times.
3. Heel Walk
Travel to one terminal of a hall and easy raise up every bit high as you can onto your heels. Walk down the hall on your heels.
When you reach the other side come down onto your pess and stand usually.
Rest. Repeat 5 times.
4. i»? Tandem Backward Walk
Travel to one terminal of a hall and topographic point one pes behind the other pes so that the heel of one pes touches the toes of the other pes.
Walk down the hall in a backward tandem walk. It is of import that with each measure the toes on one pes touch the heel of the other.
If you make a error, merely topographic point one pes behind the other and go on
down the hall. When you reach the other side, stand usually.
Rest. Repeat 5 times.
i»?
3.11 Measurement Tool
BERG BALANCE SCALE
The Berg Balance Scale ( BBS ) was developed to mensurate balance among people with damage in balance map by measuring the public presentation of functional undertakings.
It is a valid instrument used for rating of the effectivity of intercessions and for quantitative descriptions of map in clinical pattern and research.
The BBS has been evaluated in several dependability surveies.
14 points scale designed to mensurate balance of the grownup in a clinical scene.
4. DATA ANALYSIS AND INTERPREATION
The information collected was subjected to partner off ‘t ‘ trial separately for group A and group B utilizing expressions.
Formula 1
vitamin D = ? d/n
Where,
vitamin D = difference between pre trial and station trial values
vitamin D = is the average value of vitamin D
n = is the figure of topics
Formula 2:
( d-d ) 2
( n -1 )
Standard divergence SD =
Formula 3:
Standard Error ( S.E ) = SD
N
‘t ‘ calculated value = vitamin D
S.E
Formula 4:
‘t ‘ cal = vitamin D
S.E
Where, t cal is the ‘t ‘ calculated value
dI… = mean of divergence
n = entire figure of topics
s = criterion divergence
d? = amount of squared divergence
4. Independent ‘t ‘ trial
Where S =
= Mean of Control group
= Mean of Experimental group
n1 = Number of Subjects in Control group
n2 = Number of Subjects in Experimental group
S = Standard Deviation
Datas were collected from 30 patients analysed utilizing paired ‘t ‘ trial and Independent ‘t ‘ trial to happen out within group difference. All information was analysed utilizing SPSS version 10.0.
Table 1
DESCRIPTIVE DATA OF EXPERIMENTAL GROUP
S.No
Age
Year
Sexual activity
Berg Balance Scale
Pre-test
Post trial
1
48
Meter
37
47
2
50
Meter
38
45
3
46
F
36
46
4
45
F
36
45
5
49
Meter
38
47
6
48
F
35
46
7
49
Meter
37
48
8
50
Meter
37
47
9
48
F
39
48
10
48
Meter
38
47
11
47
Meter
36
46
12
50
Meter
35
46
13
49
F
38
48
14
46
Meter
35
46
15
49
Meter
39
47
TABLE-11
DESCRIPTIVE DATA OF CONTROL GROUP
S.No
Age
Year
Sexual activity
Berg Balance Scale
Pre-test
Post trial
1
47
Meter
38
41
2
46
Meter
38
42
3
46
Meter
36
41
4
47
F
37
37
5
48
Meter
35
37
6
49
Meter
39
42
7
48
F
39
42
8
48
F
38
40
9
50
Meter
36
39
10
49
Meter
37
40
11
46
Meter
38
41
12
45
F
37
40
13
47
Meter
36
39
14
47
F
39
42
15
49
F
37
41
TABLE – II1
DEMOGRAPHIC PRESENTATION OF SEX
Content
Control
EXPERIMENTAL
Male
9
10
Female
6
5
Entire
15
15
GRAPH- I
Sexual activity WISE DISTRIBUTION IN CONTROL GROUP AND EXPERIMENTAL GROUP
The above saloon graph shows, in control group 9 males and 6 females were selected ; and in experimental group 10 males and 5 females were selected.
Table Four
PRE TEST MEAN AND STD. DEVIATION OF BBS CONTROL AND EXPERIMENTAL GROUP
Group
N ( No. of Subjects )
Mean
STD. Deviation
Control
15
37.33
1.234
EXPERIMENTAL
15
36.93
1.387
Table Volt
POST TEST MEAN AND STD. DEVIATION OF BBS IN CONTROL AND EXPERIMENTAL GROUP
Group
N ( No. of Subjects )
Mean
STD. Deviation
Control
15
40.27
1.67
EXPERIMENTAL
15
46.66
1.051
GRAPH-II
MEAN DIFFERENCE OF BBS IN CONTROL AND EXPERIMENTAL GROUP
Interpretation OF DATA:
Statistical ANALYSIS OF BERG BALANCE SCALE IN CONTROL GROUP USING PAIRED ‘t ‘ Trial
Table — VI
GROUP CONTROL
Mean
South dakota
T
DF
Sig t value
Bulletin board system
PRE
37.3
1.234
10.33
14
2.1447
Post
40.27
1.67
Interpretation-Berg Balance Scale in control group-
Above tabular array shows the mean of the pre trial informations for the control group as 37.3+_1.234 ( SD ) and post trial value as 40.27±1..67 ( SD ) . The deliberate T value is 10.33. It indicates that there is important difference between pretest and station values of Berg Balance graduated table in control group.
GRAPH-III
MEAN DIFFERENCE AND STANDARD DEVIATION OF BBS IN CONTROL GROUP
Interpretation of informations
Statistical analysis of Berg Balance Scale in experimental group utilizing paired ‘t ‘ trial
TABLE – Seven
Group
Mean
S.D
‘t ‘
df
Experimental
Pre trial
36.67
1.54
27.04
14
Post trial
46.13
1.45
Interpretation – Berg balance graduated table
Above tabular array shows the mean of pre trial informations for the experimental group as 36.67± 1.54 ( SD ) and post trial value as 46.13±1.45 ( S.D ) the deliberate ‘t ‘ value is 27.04 which is greater than that of table value. It indicates that there is important difference between pre trial and station trial values of Berg balance graduated table in experimental group.
i»?
GRAPH- IV
MEAN DIFFERENCE AND STANDARD DEVIATION OF BBS IN EXPERIMENTAL GROUP
STASTICAL ANALYSIS OF BERG BALANCE SCALE OF PRE TEST VALUE USING INDEPENDENT T Trial
Table Eight
EXPERIMENTAL AND CONTROL GROUP PRE TEST VALUE
Mean
South dakota
T
DF
Bulletin board system
EXP
36.93
1.39
1.83
28
CTRL
37.33
1.23
INTERPRETATION-BERG BALANCE SCALE
CONTROL AND EXPERIMENTAL GROUP PRETEST VALUE
Above TABLE shows the mean of pre trial informations for experimental group as 36.933 ±1.39 ( SD ) the deliberate T value is 1.8310 and command group mean 37.33±1.3810 and calculated T value is 1.8310 for both experimental and control group. It indicates that there is no important difference between experimental and control group.
GRAPH-V
MEAN DIFFERENCE AND STANDARD DEVIATION OF BBS IN EXPERIMENTAL AND CONTROL GROUP USING INDEPENDENT
‘T ‘ Trial
STASTICAL ANALYSIS OF BERG BALANCE SCALE
POST TEST VALUE USING INDEPENDENT T Trial
TABLE – Nine
EXPERIMENTAL AND CONTROL GROUP POST TEST VALUE
Mean
South dakota
T
df
Bulletin board system
EXP
46.6
1.0521
12.6626
28
CTRL
40.27
1.6701
INTERPRETATION- BERG BALANCE SCALE
CONTROL AND EXPERIMENTAL GROUP POST TEST VALUE
Above tabular array shows the mean of station trial informations for experimental group as 46.6 ±1.058387 ( SD ) the deliberate T value is 12.6626 and command group mean 40.27±1.6701 and calculated T value is 12.6626 for both experimental and control group. It indicates that there is a important difference in experimental group value than control group
GRAPH-VI
MEAN DIFFERENCE AND STANDARD DEVIATION OF BBS IN POST TEST VALUES OF EXPERIMENTAL AND CONTROL GROUP USING INDEPENDENT ‘T ‘ Trial
5. Result
Effectiveness of Control Group ( Medical intervention )
While comparing the pre-test and station trial values of control group utilizing Paired ‘t ‘ trial, the deliberate T value is 10.33 whereas the tabular array value is 2.145, it states that there is important difference between the pre-test and post-test values of control group. When comparing the average values of both, the station trial mean value is 1.67 which are greater than the pre trial mean value 1.234. Hence it confirms that there is a important betterment group.
Effectiveness of Experimental Group ( Balance exercising with medical intervention )
While comparing the pre-test and station trial values of experimental group utilizing Paired’t ‘ trial, the deliberate value is 31.8590646 whereas the tabular array value is 2.145. Since the deliberate value is more than the critical value, it states that there is important difference between the pre-test and post-test values of experimental group. When comparing the average values of both, the post-test mean value 46.6 which is greater than the pre-test mean value 36.933. Hence it confirms that there is a important betterment in post-test experimental group than pre trial experimental group.
6. Discussion
Diabetess Mellitus is a Chronic status which encroaches about all the systems in the organic structure. Diabetic neuropathy is a complication of long standing diabetes, which affects nervousnesss of the organic structure. Diabetic neuropathy can impact all the tissues and the variety meats of the organic structure. Approximately about 60-70 % of the people with diabetes suffer from neuropathy and the oncoming can be at any clip in life. The incidence of neuropathy in diabetic patients increases with the period of diabetes.
This survey was an experimental attack, which studied the effectivity of balance exercising in diabetic neuropathy patients. The result was measured utilizing Berg Balance Scale. It has been shown to a valid and dependable tool for the measuring of balance by measuring the public presentation of functional undertakings. The control group was given medical intervention and the patient besides given balance exercising in experimental group.
Harmonizing to Shahin Goharpey, diabetic neuropathy consequences in functional instability which cause these patients to danger of falling during activities of day-to-day life and becomes more terrible as the badness of neuropathy aggravates. Balance exercising improves clinical steps of balance in patients with diabetic neuropathy.
Loss of force per unit area sensitiveness was independently associated with the hazard of falling more than one time a twelvemonth and histories for 3- 6 % of relationship between diabetes and falling.
Based on above survey, the present survey concluded that balance preparation to be an effectual agencies of cut downing frequence of autumn in patients with diabetic neuropathy.
Mechanism
The mechanism by which balance preparation affect the balance of diabetic neuropathy is due to,
1. During exercise whole organic structure O ingestion additions in the musculuss.
2. Addition in the concentration of Na+ / K+ adenosine triphosphatase ( ATPase ) pumps.
3. Exercise works to cut down insulin opposition which lowers blood sugar degrees. So heavy insulin opposition will set less strain on the organic structure to do insulin.
4. Exercise is helpful in keeping strength, mobility, map and besides provides stableness
7. Decision
The survey concludes that balance exercising seemed to be good in bettering balance and thereby cut downing the frequence of autumn in patients with diabetic neuropathy.
LIMITATIONS AND SUGGESTIONS
Restriction
Study was conducted for a short period of clip.
The survey assessed merely short term advancement of the patients.
Since survey clip was short merely limited sample since could be considered for the survey.
Suggestion
To set up the efficaciousness of the intervention a big sample size survey is required.
To do the consequence more valid a long term survey may be carried out.
The same survey can be done by modifying the exercising by increasing the complexness.
The same survey can be done by increasing the exercising by its repeats.
The same survey can be carried out in males and females individually.

Diabetes Mellitus Syndrome Chronic Hyperglycemia Health And Social Care Essay

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Walking Dead Syndrome

Walking Dead Syndrome.
THE WALKING DEAD SYNDROME English 150 Instructor: S. Jone November 7, 2011 The Walking Dead Syndrome Introduction The Walking Dead syndrome is considered a rare disease. I believe everyone in this existence has a purpose on this vast place we call earth. However, there are people diagnosed with a syndrome who believe they have no soul or convinced themselves they are dead. The “Walking Dead Syndrome” is also commonly known as “Cotard’s Syndrome”. In this paper, I will refer this syndrome as “Cotard’s syndrome”.
Cotard’s syndrome is linked with other mental illnesses which could explain a person’s state of mind of feeling non-existent in society. I will further discuss eight aspects of this syndrome: defining the Walking Dead Syndrome, defining mental illness, description of several mental illnesses associated with this syndrome, classifications of Cotard’s syndrome, analysis of patients, diagnosis of syndrome, and types of treatments available for patients. Defining Walking Dead Syndrome or Cotard’s Syndrome
Many people I discussed this topic with never heard of the “Walking Dead Syndrome”. The Walking Dead Syndrome was first created by French neurologist, Jules Cotard, hence, named the “Cotard’s Syndrome”. He was a French neurologist who first described this psychiatric condition. First reference to the syndrome was made in the year 1880, when Jules Cotard gave a lecture in Paris. In this lecture, he described various degrees of the syndrome, while he said that a person who resorts to despair and self-hatred begins in the early stages of this disorder.

With deterioration, the person might go to the extent of denying the very existence of himself or herself. There are detached from the sense of existence of self (“Cotard Syndrome” 2010). Patients portray themselves similar to the concept of “zombies”. Hollywood has portrayed horror and science fiction based movies on “zombies” or the “walking dead”. In the movies, zombies are typically mean and fond of human flesh, they groan and cannot talk, have incredible strength, and display rotting flesh.
A zombie is physically identical to a normal human being, but completely lacks conscious experience. If we suddenly lost our minds, or consciousness our bodies might continue to run on for a while, our hearts might continue to beat, we might breathe while asleep and digest food. But without the contribution made by minds, behavior could not show characteristically human features. In the Urban Dictionary, 1999-2011, a zombie is defined “as deceased human being who has partially returned to life due to undeterminable causes.
The brain retains base facilities, namely gross motor function. In its near-mindless state, it grasps no remains of emotion, personality, or sensation of pain. In rare cases, some of the reanimated have reflexively preformed routine activities from their past lives”. The people diagnosed with Walking Dead Syndrome have similar portrayals including not having internal organs and smelling of rotting flesh. A hypothetical analogy can be explained when most of us have woken up after a really good night out.
Our first drive in the morning was motivated by a desire for food and coffee. If we as a society experience a chemical or radiological contamination, we might be experiencing the hangover from hell. Our higher thought would be destroyed, the neural system would be degraded, and leave just the body running on its primary functions. Defining Mental Illness Since the beginning of man, I think there has been mental illness, and chemical imbalance generates a huge part, and some people just do not have the ability to use parts of their brain for reason and logic.
According to to Sorrentino, Wilk, and Newmaster (2009), a mental illness can be: “caused by a combination of genetic, biological, personality, and environmental factors, is a disturbance in a person’s ability to cope with or adjust to stress; the person’s thinking, mood, and behaviours are affected, and functioning is impaired …mental illnesses affect people of all ages, culture, and educational and income levels. The onset of most mental illnesses occurs during adolescence and young adulthood” (p. 641). Most mental illnesses are brought on by the stresses of life, money, property, and consumption.
Having a mental illness varies from person to person and if you cannot go about your day as you normally would due to a condition then it is a mental illness. An example would be having an “anxiety disorder”, and if you cannot leave your house anymore due to petrifying fear, then there is clearly a problem. Unless of course you cannot recognize that you are having problems and you are posing a threat to yourself or others, then you can be forcibly placed under the guidance of a psychologist. Mental illness can be contributed to either biological, psychological, and environmental factors.
The biological factors can be attributed to genetics or “mental disorders tend to run in families, suggesting a hereditary factor…the number of close relatives a person has who suffer from depression or other mood disorders is the best predictor of the likelihood that the individual will develop a mood disorder” (Boyd, Johnson, Bee, 2009, p. 385). In addition, psychological aspects can be contributed to emotional, physical, or sexual abuse, and the environmental causes can be defined as a person living in poverty or substance abuse. Mental Illnesses Associated with Cotard’s Syndrome
People diagnosed with the “Cotard’s Syndrome” have been treated for a mental illness or combination of bi-polar, delusions, schizophrenia, and schizoaffective disorder, to name a few. The major mental illnesses are painful, pervasive, disruptive and usually disabling. Firstly, a “bi-polar disorder” is defined as “a brain disorder that causes unusual shifts in a person’s mood, energy, and ability to function” (Sorrentino, Wilk, Newsmaster, 2009, p. 651). Whereas, “delusions” are the “false beliefs that are firmly held” (Purse, 2011). An example is a person who has grandeur delusions or has paranoid tendencies.
In the grandiose subtype, the person is convinced that he has some great talent or has made some important discovery, they have an inflated sense of self-worth. In addition, their delusions center on their own importance, such as believing that they have done or created something of extreme value or think they have a “special mission”. There is reference to another type of delusion known as “nihilistic delusions”. This type of delusion describes a person “focused on the individual’s body, including loss of body parts, being dead, or not existing at all” (Debruyne, Portzky, Peremans, & Audenaert, 2011).
Furthermore, Cotard syndrome created a new type of depression which “is described as anxious melancholia, ideas of damnation or rejection, insensitivity to pain, delusions or nonexistence concerning one’s own body, and delusions of immorality” (Debruyne, Portzky, Peremans, & Audenaert, 2011). This type of delusion is a major attribute of Cotard’s syndrome. Thirdly, “schizophrenia” which “is an extremely complex mental health disorder characterized by delusions, hallucinations, disturbances in thinking, and withdrawal from social activity” (Sorrentino, Wilk, Newsmaster, 2009, p. 55). News and entertainment media tend to link mental illnesses including schizophrenia to criminal violence. Most people with schizophrenia, however, are not violent toward others but are withdrawn and prefer to be left alone. Lastly, “schizoaffective disorder” is described as a “person having symptoms of both schizophrenic and bipolar disorder” (Purse, 2006). Some disorders will cause parts of the brain to stop performing their normal functions. These can leave people out of control and disoriented (not knowing what they themselves are doing). Classifications of Cotard’s Syndrome
In its early stages, Cotard’s syndrome is characterized by vague feeling of anxiety with a varying time p from weeks to years. This anxious state gradually augments and can result in nihilistic delusions where denial of life or denial of body parts are the prominent features. The patient loses sense of reality. Despite the delusion of being dead, these patients show an increased tendency to automutilation (self harm) or suicidal behaviour. (Debruyne, Portzky, Peremans, and Audenaert, 2011). A case studying involving 100 patients, in Debruyne, Portzky, Van den Eynde, and Audenaert, (2009) reveal three types of Cotard’s syndrome.
The first is a form of “psychotic depression” in which anxiety, melanchonlia, delusions of guilt, and auditory hallucinations are the more prominent features. The second class is “Cotard’s syndrome Type I”, which is associated with hypochondriac and nihilistic delusions. The third type is “Cotard’s syndrome Type II”, which includes anxiety, depression, delusions of immortality, nihilistic delusions and suicidal behaviour are characteristic features”. However, in Debruyne, Portzky, Peremans, and Audenaert, 2011, a case study conducted in 1999, identified three stages of Cotard’s syndrome.
The first stage, germination stage, is characterized by important hypochondriac cenesthopathy and depressive mood. A diagnosis of Cotard’s syndrome cannot be made in this stage yet. In the blooming stage, the characteristic features of Cotard’s syndrome (nihilistic delusions, delusions of immorality together with anxiety and negativism) are seen. The last stage, the chronic stage is differentiated in two forms: one with persistent emotional disturbances (depressive type) and the second where depressive symptoms are less prominent (paranoid type) (as cited by Yamman, 1999).
The two classifications described above have assisted in diagnosing of Cotard’s syndrome. The similar features displayed are nihilistic delusions, depressive mood, and anxiety. Analysis This syndrome does not affect a specific category of people. A study of 100 patients, revealed that “Cotard’s syndrome was diagnosed in 2 of 349 patients…taking into account only severely depressed older adult patients. In addition, the average of age of person studied was 52 years of age, however, the study also suggested that Cotard’s was occasionally described in children and adolescents (Debruyne, Portzky, Van den Eynde, Audenaert, 2009).
Furthermore, according to Wani et al. , (2008), “this syndrome is typically related to depression and is mostly found in middle-aged or older people. In the analysis the following results were displayed: “depressive mood (89%), nihilistic delusions (69%), anxiety (65%), delusions of guilt (63%), delusions of immortality (55%), hypochondriac delusions (58%)” (Debruyne, Portzky, Peremans, and Audenaert, 2011). Diagnosis The diagnosis reveals a psychological and neurological aspect of Cotard’s syndrome. The “depersonalization phenomenon” as described in Debruyne, Portzky, Van den Eynde, and Audenaert, 2009, is referred to using German erminology leib (body for me) and korper (body as such), korper becomes more prominent than leib and the body less associated with the self (leib), depersonalization onset can then occur. However, in depersonalization, the patient feels as if he or she is dead (in difference of affect), whereas in Cotard’s syndrome, the patient is convinced that he or she is dead (lack of feeling). Cotard’s syndrome is often associated with parietal lobe lesions. Compared with controls, patients with Cotard’s syndrome have more brain atrophy in general and more median frontal lobe atrophy in particular.
Cotard’s syndrome may be associated with multifocal brain atrophy and medial frontal lobe disease. Neurological assessments were performed and findings resulted in patients affected by “parietal brain dysfunction” and structural brain abnormalities. Recent discoveries have indicated that Cotard’s syndrome was associated with multifocal brain atrophy and interhemispheric fissure enlargement. The interhemispheric fissure enlargement means “parietal lobe lesions” (Joseph and O’Leary, 2011) or bending in the frontal and occipital regions and this abnormality also been observed in schizophrenic patients.
Others have described and enlargement of the third and lateral ventricles. In one patient, the patient was diagnosed with a schizophrenia disorder and a left sided hypoperfusion in the temporal, parietal and frontal lobes. The medical term of hypoperfusion is defined as a “decreased blood flow through an organ” (Meriam-Webster, 2011). In addition, the patient experienced improvements of the inferior frontal and left hypoperfusion and there was evidence of decreased hyperprofusion of the left temporal lobe…” (cited in Debruyne, Portzky, Van den Eynde, and Audenaert, 2009).
Treatments There are several methods utilized to treat mental health struggles. A patient can seek professional assistance by psychology or psychiatry therapy and/or the utilization of medication. If you lived in the 16th century with any undefined mental disorder, you were considered as “possessed by the Devil” and cast away to some godforsaken monastery dungeon in which monks would constantly pray for and exorcise you. The Catholic Church they used a methodical guidebook to describe all behavioral aspects and associations of witchcraft, satanism, etc. nd utilized this upon people who were suffered with mental or behavioral maladies, and it was not commonly understood in the Medieval and Renaissance periods. In the medieval ages, they were burned because they thought demons haunted the mentally ill. In later years, we willfully experimented on them, cutting into their bodies and brains to “fix them”, this was called, trepanation. The “evidence of trepanation has been found in prehistoric human remains from Neolithic times onward.
Cave paintings indicate that people believed the practice would cure epileptic seizures, migraines, and mental disorders” (Wikipedia, 2011). It is really disgusting and is the major reason that even today it is to some a badge of humiliation instead of just an illness. Complete recovery may occur spontaneously and suddenly as onset of Cotard’s syndrome. There are several reports of successful pharmacological treatment of Cotard’s syndrome. Electroconvulsive Therapy (ECT) is considered an important treatment option in Cotard’s syndrome.
It is noted, in Debruyne, Portzky, Van den Eynde, Audenaert, 2009, that young patients use of mood stabilizers should be considered because Cotard’s syndrome in this population is often part of a bipolar disorder. Successful treatment with ECT and the patient with underlying major depressive disorder resulted in recovery of left and right temporal hypoprofussion and normalization of profusion in the frontal cortex was reported after treatment with antidepressants (Debruyne, Portzky, Peremans, and Audenaert, 2011). Please be aware that people who have true mental illnesses do suffer.
They want more than anything to be able to feel and function like other people and they will actively seek help. The reality is that certain medications and treatments help those who are suffering from these conditions. Conclusion Mental illness is not a modern invention. The mentally ill have been recognized in one form or another by every culture we have a record of. How they were perceived and what their value is what has largely changed. Some people do not retreat into their minds as much as they are supposed to, while others spend all their time there.
What we eat and breathe and drink affects our health and our brain, and a healthy individual’s brain tends to have more to work with and develop all the right chemicals and nerve sheaths. A good parent with their strong sense of empathy realizes that their child is a thinking, growing human being and will always need that light touch that points them in the “right direction” and prevent them from getting “lost”. The right nature and nurturing are essential for a healthy development. Some cases of these disorders I believe could be a simple lack of the ingredients to solve this chemical imbalance.
Given that our brain is constantly changing accordingly with the times, a chronic chemical imbalance quickly becomes more than just that, as the brain has grown and changed around this shortcoming. The kind of understanding you wish people had for those with mental disorders would be a universal understanding for all if people would look into themselves and observe their own thoughts and behaviors. We are our best test subjects since we have full access to all the “data”, and by observing ourselves totally (mentally, developmentally, chemically) we can apply our understanding to others and learn from the experience.
People need to care about how people’s minds work in general, understanding “you guys” would come with the turf, and communication with our angry neighbors would be much more effective since we’d all see where everyone is coming from. Philosophers have long contemplated human happiness, and how to live a “good” life, in harmony with our own nature. The problem is that humans do not really know what makes them happy, and what they think will, or will not, and instead they find contempt and superficial pleasures they believe will satisfy them.
As a result, some people will not live a good and peaceful life that satisfies the majority of people. The fact is not everyone needs medication, but there are those who do. Some need it temporarily, some for a lifetime. Some simply need therapy, and some benefit from dietary changes. I believe understanding is the highest ideal we should seek to attain. Understanding and being honest with ourselves about ourselves and applying our own understanding to others may help us see that we are not as different as we’d like to believe.
I believe that sense of commonality with all human beings can generate empathy, compassion and ultimately peace in all of us. It is when we categorize each other, ourselves, and place value on those categories then we breed hatred, ignorance and fear. References Boyd, D. , Johnson, Paul, Bee, Helen (2009). Lifep Development. (4th Canadian Edition). Toronto: Pearsons Canada Inc. Cotard Syndrome. (2010). Disorders Central. Retrieved October 10, 2011, from http://www. disorderscentral. com/cotard-syndrome. html Debruyne, H. , Portzky, M. Peremans, K. , ; Audenaert, K. , (2011). Mind and Brain The Journal of Psychiatry. Retrieved October 6, 2011, from http://content. yudu. com/Library/A1t5r8/MindampBraintheJourn/resources/73. htm Debruyne, H. , Portzky, M. , Van den Eynde, F. , ; Audenaert, K. (2009). Cotard’s Syndrome: A Review. Current Psychiatry Reports. Retrieved October 6, 2011, from University of Calgary On-line Resources: http://www. springerlink. com. ezproxy. lib. ucalgary. ca/content/f43j790n7161432m/ Hypoperfusion. (2011). Merriam-Webster Dictionary.
Retrieved November 5, 2011, from http://www. merriam-webster. com/medical/hypoperfusion Joseph AB, and O’Leary DH. (2011). Brain atrophy and interhemispheric fissure enlargement in Cotard’s syndrome. PubMed. gov. Retrieved November 6, 2011, from http://www. ncbi. nlm. nih. gov/pubmed/3759917 Purse, Marcia. (2011). Delusions. About. com. Retrieved October 6, 2011, from http://bipolar. about. com/od/definingbipolardisorder/g/gl_delusions. htm Purse, Marcia. (2006). Schizoaffective Disorder. About. com. Retrieved October 6, 2011, from http://bipolar. about. om/od/glossary/g/gl_schizoaffect. htm Sorrentino, Sheila A. , Wilk, Mary J. , and Newsmaster, Rosemary (2009). Mosby’s Canadian Textbook for the Support Worker. (2nd Canadian Edition). Toronto: Elsevier Canada Urban Dictionary. (1999-2011). Zombie. Retrieved November 6, 2011, from http://www. urbandictionary. com/define. php? term=zombie Wani, A. Z, Abdul, W. Khan, Aijaz, A. Babe, Hayat, A. Khan, Qurat-ul, A. Wani, and Taploo, Rayneesa (2008). Cotard’s syndrome and delayed diagnosis in Kashmir, India. International Journal of Mental Health Systems.

Walking Dead Syndrome

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Noonan Syndrome

Noonan Syndrome.
Noonan Syndrome Nicole Mitchell Dr. Hendricks Principles of Biology 1114 April 19, 2013 Mostly everyone in the world has heard of some type of genetic disorder. But most people haven’t even heard or understand about Noonan Syndrome. Noonan syndrome is a genetic disorder characterized by distinctive facial features, developmental delay, learning difficulties, short stature, congenital heart disease, renal anomalies, and bleeding difficulties. Noonan syndrome affects a good percent of the world and may happen to anyone. Noonan syndrome has many key symptoms and very few certain treatment options.
Noonan syndrome used to be referred to as the male version of Turner’s syndrome (and is still sometimes described in this way); however, the genetic causes of Noonan syndrome and Turner syndrome are distinct. The principal features of Noonan disorder include congenital heart defect (typically pulmonary valve stenosis) also ASD, hypertrophic cardiomyopathy, short stature, learning problems, pectus excavatum, impaired blood clotting, and a characteristic configuration of facial features including a webbed neck and a flat nose bridge.
The syndrome is named after Dr. Jacqueline Noonan. Mutations that cause Noonan syndrome alter genes encoding proteins with roles in the RAS-MAPK pathway, leading to pathway deregulation. Noonan syndrome is a relatively common genetic disorder with an estimated prevalence of 1 in 1000 to 1 in 2500 births. If someone knows enough about this disorder, they may be able to spot them out. However, people who have Noonan syndrome have problems not only on the outside but mainly on the inside. Noonan patients have to battle a lot mainly when it comes to their heart.

Cardiomyopathy is more than fifty percent of the problem and the main reason of death. To explain for a moment, Cardiomyopathy can cause heart failure and sudden cardiac death. Not only do they have to worry about cardiomyopathy, they have atrial septal defect (ASD). ASD only appears in ten percent or less of Noonan patients and may be so small it will not affect the patient to an extreme level. To elaborate, ASD allows oxygen to get to the tissues, organs, and to each side of the heart. Not only does Noonan disorder have problems in the cardio area, but also in the gastrointestinal system.
Infants up to adults may have problems with their appetite, digestive issues, forceful vomiting, and difficulties swallowing. Considering normal people eat through their mouth, it can be very hard or unpleasant for a child with Noonan syndrome to eat and not only eat but to keep it down. Another big issue with Noonan patients are they tend to have a hematologic symptoms like easy bruising, blood clotting disorders, and partial deficiency of Factor VIII:C, XI:C, and XII:C. Not only do I feel bad for the patient themselves, but whoever has to take care of them.
Since no one has x-ray vision except for Superman, it comes in handy to know the external signs of Noonan Syndrome. Noonan syndrome sounds like a few disorders combined. Their body stature and posture is very unmannered. They normally have a short stature, cervical neck or spine, scoliosis, a depression or outward breast bone, and a very low muscle tone. Their head usually has excess skin on the back of the neck, a low hairline in the back and high hair line in the front. Their heads are usually large and triangular shaped. They have a short and/or webbed neck.
Their eyes are unusually very wide and their eyelids droop excess fully. Over ninety percent has low set ears, backward rotated ears, thick outer rim of the ear and sometimes incomplete ear folds. They have a deeply grooved top lip line and their fingers are bluntly ended, sometimes extra padded (on toes as well), and may have poor tongue control. Sometimes we do not even notice most of these body parts, but now that people know they often look. Treatment of the symptoms and complications that occur with Noonan syndrome depends on their type and severity.
Many of the health and physical issues associated with this syndrome are treated just the way they are in the general population. The heart will be treated with certain drugs and surgery may be necessary. Since there are no many different factors with Noonan syndrome children are checked multiple times a year. Family doctors or the doctors of the parents choosing focus on the blood chemistry, thyroid function, bone growth and hormone levels. If a child’s growth hormone levels are insufficient, growth hormone therapy may be a treatment option.
For the other factors like learning disabilities, vision care, and etc. , they are treated like every other special child and normal child. If the child does, and most likely will, have a learning disability then if caught early on doctors can find certain centers that teach on speech and the learning process. When you look up or study these genetic disorders, you learn that most of them are really not so rare. I have heard about Noonan Syndrome before but I never knew how common it was. I only learned that it is a very unique disorder and sounds very much like Turner’s syndrome.
It makes me sad to believe that parents have to suffer so much through all of these treatments and never knowing really what they can do. They may wake up one morning and their child has gone into cardiac arrest. It’s a sad disorder and there is no treatment for the Noonan syndrome itself, but only what they can do for anyone else. Not saying that the medicine today is not good enough, but maybe not fast enough or efficient enough for a child or adult who has so many more problems to deal with. I can only imagine that they person will be required to take a minimum of fifteen pills a day depending on how many symptoms they have.
Noonan syndrome is a terrible genetic disorder that affects both the inside and outside of every patient. It is a roller coaster ride of a life and never know what will or may happen once the child or adult falls asleep. It is common everywhere in the world and happens between one thousand and two thousand five hundred children a year. Even though it is very similar to Turners Syndrome, this happens in both males and females. Most children with the disorder look alike and have most of the same symptoms. It is unlikely to have other symptoms, but with this genetic disorder anything is possible.
Signs or symptoms increase all of the time and there is no set guideline for the things that may occur. Work Citied Romano, A. , MDA, and Allanson, J. , MDb. “Noonan Syndrome: Clinical Features, Diagnosis, and Management Guidelines. ” Google Scholar. 27 September , 2010. Pediatrics Vol. 126 No. 4 p. 746 -759. Web. 12 April , 2013. http://pediatrics. aappublications. org/content/126/4/746. full. Lisbona, P. and Moreno, M. “Noonan Syndrome” Google Scholar. March 2009 vol. 18 no. 3 p. 267-269. Web. 09 April, 2013. http://lup. sagepub. com/content/18/3/267. abstract. Pediatr, C. Noonan Syndrome: An Update and Review for the Primary Pediatrician. ” Google Scholar. September 1994 33:p. 548-555. Web. 12 April, 2013. http://cpj. sagepub. com/content/33/9/548. full. pdf+html Connor, W. and Noonan J. “Noonan syndrome: A clinical description emphasizing the cardiac findings. ” Wiley Online Library. 19 JAN 2011. Japan Pediatric Society. Web. 10 April, 2013. http://onlinelibrary. wiley. com/doi/10. 1111/j. 1442-200X. 1996. tb03443. x/abstract. Baraitser, M. and Patton, M. “A Noonan-like short stature syndrome with sparse hair. ” Journal of Medical Genetics. 23:2. Web. 08 April, 2013.

Noonan Syndrome

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Tourettes Syndrome in Children

Tourettes Syndrome in Children.
Tourette’s syndrome, also called Tourette’s disorder is named after the neurologist, Gilles de la Tourette. Sometimes it is referred to as GTS but more often it is simply called Tourette’s or ‘TS’. It is an inherited neurological disorder marked by movement-based (motor) tics which are abrupt, repetitive, stereotyped, non-rhythmic movements, as well as vocal (verbal or phonic) tics which are involuntary sounds produced by moving air through the nose, mouth, or throat. Tourette’s is defined as part of a spectrum of tic disorders, which includes transient and chronic tics.
This disorder may appear in multiple family members, and often appears (co-morbid) with other behavioral disorders, in particular – “obsessive-compulsive disorder (OCD) and attention deficit hyperactivity disorder (ADHD)” (Hawley 2008). People with this disorder have normal life expectancy and intelligence, but symptoms can lead to decrease in normal activities (Walkup, Mink & Hollenbeck 2006). Tourette’s syndrome, as described in the psychiatric diagnostic tool DSM-IV-TR criteria is “associated with distress or social or functional impairment” (Hawley 2008). Onset and Diagnosis.
The most common first sign to alert people to visit the doctor for a possible presence of Tourette’s is a facial tic such as “rapidly blinking eyes or twitches of the mouth” (NTSA 2009). Unintended, involuntary sounds such as throat clearing, shrugging or tics of the limbs may be initial signs but in certain case, although rare, the symptoms become abruptly with multiple symptoms of movements and sounds. Chronic tic disorder is diagnosed with the presence of single or multiple tics, and the presence of motor or phonic tics (but not both) which is present for a year or more.

On the other hand, Tourette’s which falls under the category of above is diagnosed when there are multiple motor tics occurring at the same time with one phonic tic and is manifested for more than a year. As a general rule, simple motor tics like blinking are first noticed on the child at around 5-10 years old, while vocal tics start manifesting after 8 years old but before the child is 15 years old. Symptoms of the disorder can be seen in infancy but this is a rarity. As a rule, the symptoms may come and go and children show identifiable signs at round 7 years old (Hawley 2008), and before 18-21years old (Black 2007).
Studies found the most onset was between 9-14 years of age (Leckman 2003, Black 2007). Another study showed that tics started below 18 years, but 5 relatives had an onset after the age of 21 years. Affected persons will “blink, jerk, grunt, clear their throats, swing their arms, grasp or clasp others, have obsessive-compulsive behaviors or use verbal expletives (coprolalia) uncontrollably” (Tabers 2001, 2207). In some cases, people suffering from Tourette’s can control the verbal expletives in public but they will express it vigorously once they are in private.
Coprolalia, “the uncontrollable utterance of socially objectionable or taboo words or phrases” is the most popular symptom of Tourette’s but it is not required for a diagnosis hence about 90% of patients afflicted with it only Tourette’s does not have coprolalia. The most common, initially noticed motor tic is eye blinking and the vocal tic is repetitive throat clearing (Black 2007). The disorder often persists throughout the individual’s lifep but severity peaks in adolescence and thereafter decreases to a point that it is almost not bothersome to the person.
This average though can be very misleading because some form of fluctuation or recurrence have been documented although it is not severe. There have also been rare cases that reported a recurrence of tics that is bothersome enough to seek medical attention, and have had to maintain lifelong treatment due to progressively worsening of tic activity (Black 2007). Prevalence. Tourette’s syndrome used to be known as a rare condition but it is now contended by doctors and psychologists that it may be more common but misdiagnosed because some cases are so mild that patients and their families discard it as being an oddity rather than Tourette’s.
Most children with TS have mild, barely bothersome, non-disabling symptoms, and it is difficult to distinguish the signs of the disorder as opposed to a child acting out such as Mimicking others, blinking being viewed as tormenting someone who may have done so because they wear glasses, or by doing things that others would view as the child just trying to get attention, therefore, medical attention is not a thought to the parents of the child who is doing these things.
In some patients the tics improve and disappear as they grow older; hence, they never seek medical attention. The estimated prevalence is 0. 7-4. 2% (Hawley 2008) based on children checked in public schools. Tourette’s is known to be familial and its prevalence rate in first-degree relatives is 5-15% (about 10 times the prevalence rate in the general population). Chronic motor tics occurring, without vocal tics has also been documented as being common in relatives (Black 2007).
In special education programs, 26% of students identified tics, as compared to 6% of students in mainstream classrooms led to identification of co-morbidity with having symptoms of TS included ADHD and OCD (Hawley 2008), impulse control disorders, anxiety and mood disorders, as well as difficulties with living and adaptation (Walkup, Mink & Hollenbeck 2006). It is estimated that 1 in 10 children per 1,000 have Tourette’s disorder, and as many as 1 per 100 people may have tic disorders.
In children, male to female ratio varies from 2-10:1 (Hawley 2008), boys have an increased prevalence for chronic tics compared to girls in exhibiting 5:1 ratio, although some studies show between 2:1 and 10:1 ratios (Black 2007). If OCD data is included as a variant of Tourette’s, their quantities added to the total, the ratio between boys and girls become equal (Hawley 2008). Causes. Environmental factors may contribute to the cause but up to now exact causes of the disorder is still are not known.
The clinical phenomenon are very similar across social classes, ethnicity and culture which suggests a genetic basis and the disorder has been reported globally (Hawley 2008). As children pass through adolescence, the tics decrease in severity and it is extremely rare for Tourette’s to persist in adulthood. Whether the resolution is a compensation of the neuro system or a resolution of the underlying pathology is unclear (Hawley 2008).
Adults who show signs of the disorder are likely to have shown symptoms since childhood, although these may have been so mild that they were generally unnoticed and undiagnosed. In the US though, most diagnosed patients being examined at research centers and affiliated with lay organizations are white. But this does not necessarily mean that Caucasians have a predisposition, it may merely be due to differences healthcare-seeking behaviors. A non-genetic cause may also exist and is still under research and investigation.
Additional evidence is being gathered regarding the differences in severity between affected twins with the twin having experienced peri-natal complications experiencing increased symptom severity (Hyde 1992, Black 2007). Also garnering much attention is the theory that Tourette’s syndrome may be caused by an abnormal immune response to streptococcal infection. In several documented cases, tics began suddenly after a streptococcal infection. As a result of this the case definition for a “post-streptococcal autoimmune neuro-psychiatric disorders” came into being (Snider 2003, Black 2007).
The difference between other movement disorders such as choreas, dystonias, and dyskinesias and that of Tourette’s – these are “temporarily suppressible, non-rhythmic and more often than not are preceded by a premonitory urge” (Black 2007). Just before an onset, an afflicted individual feels an urge that is similar to one felt before a sneeze or an itch that needs scratching. This is often pictured as a buildup of tension and energy which they are then able to consciously release so the sensation is relieved.
It is further described as “something stuck in one’s throat, a localized discomfort in the shoulders that leads to the need to clear one’s throat or shrug the shoulders” (Hawley 2008). The actual tic is eventually felt as relieving this tension or sensation, similar to clearing the throat or shrugging the shoulder. This is how “premonitory sensory phenomena” or premonitory urges are described by sufferers. Medication and Treatment. Often, medication is unnecessary and a safe and effective medication for each and every case of tic is yet to be introduced.
There have been medications as well as therapies that help to reduce certain types of tics, but not cure it. In general, the medical management of Tourette’s is the treatment of coexisting behavior symptoms, change in diet, patient and family education. The patient and family are educated regarding how to effectively handle the manifestations of the disorder, and if an effective adaptation is made, they can avoid the use of medications. Medication is only considered when there is substantial interference with social and academic performance, as well as activities of daily living.
The target is not for completely eliminating the symptoms but merely to alleviate the social embarrassment and discomfort so as to improve the social and academics life of the child. Various pharmacological agents are used to reduce the symptoms’ severity but it only treats the symptom and often the medications are have neurological effects whereas it has been argued that the disorder is a neurobiological condition. No curative or preventive treatments are atill available for this neurobiological or even biological aspect.
There is a growing movement to go against medications because this being a chronic disorder, the goal should be long-term benefit rather than quick improvement at any cost. Families are also getting increasingly worried that the medications might have a detrimental effect in their children, that perhaps in the end, it ‘damages’ them rather than helping. It has been Resources for the child and families are available in several way which include educating students and school personnel regarding the nature the syndrome as well as improving the school environment will help the patient to avoid pharmacotherapy.
Parents and families members of a child who has TS can turn to agencies such as the National Tourettes Association, counseling with the doctor’s, videos, and self help books. Reference List Black, Kevin J.. , Webb, Heather. Neurology: Pediatric Neurology: Tourette Syndrome and Other Tic Disorders. Mar 30, 2007. Available from eMedicine Specialties at http://emedicine. medscape. com/article/1182258-overview Hawley, Jason S. , Darnall, Carl R. , Gray, Sharette K. Pediatrics: Developmental and Behavioral – Tourette Syndrome. 23 June 2008.
Available from eMedicine Specialties at http://emedicine. medscape. com/article/289457-overview. National Tourette Syndrome Association, Inc. Tourette Syndrome: Frequently Asked Questions Website http://www. tsa-usa. org. Available at http://www. tsa-usa. org/Medical/Faqs. html. 2009. Taber’s Cyclopedic Medical Dictionary. Tourette’s Syndrome. (pp. 2207-2208). Philadephia, PA. F. A. Davis Company. 2001. Walkup, John T. , Mink, Jonathan W. , Hollenbeck, Peter J. Edition: Tourette Syndrome. Lippincott Williams & Wilkins. 2006.

Tourettes Syndrome in Children

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Rubenstein-Taybi Syndrome Research Paper

Rubenstein-Taybi Syndrome Research Paper.
Rubinstein- Taybi Syndrome: A Physical and Educational Perspective Rubinstein- Taybi Syndrome: A Physical and Educational Perspective When speaking of terms of diseases of a rare nature, Rubinstein-Taybi Syndrome is a definite mention. According to Joseph G. Morelli, MD, Rubinstein-Taybi Syndrome is characterized as, “a genetic disease that involves broad thumbs and toes, short stature, distinctive facial features, and varying degrees of intellectual disability” (2007). The condition itself is so rare that is occurs only about 1 in 125, 000 newborn babies (Rubinstein, 2012).
The cause of Rubinstein-Taybi Syndrome can be attributed to a defect in the CREBBP and EP300 genes. The CREBBP gene provides instructions for making a protein that helps control the activity of many other genes. This protein, called CREB, plays an important role in regulating cell growth and division and is essential for normal fetal development. If just one copy of the CREBBP gene is deleted or changed, cells make only half of the normal amount of CREB binding protein (Rubinstein, 2012). The EP300 gene, unlike the CREBBP gene, controls protein development before and after the birth.
In many of the cases of Rubenstein-Taybi Syndrome, no mutation is detected in either the CREBBP or the EP300 gene. In these cases, the case is unknown, but it is suspected that another unknown gene is responsible. Diagnosis of Rubinstein-Taybi Syndrome can create a serious disadvantage for a student in the classroom, for which a teacher must be willing to accommodate. Immediately after birth, the symptoms of Rubinstein-Taybi Syndrome can be present. Some of the more recognizable symptoms at birth include broadening of the thumbs and big toes.

Although these are a few of the symptoms, the symptoms appear on a large spectrum, ranging from constipation to an absent kidney. Over 80% of children with Rubinstein-Taybi Syndrome have some type of eye abnormality including crossed eyes, cataracts, and tear duct obstruction. Glaucoma may be present at birth or in early life, which can result in blindness if left undetected (Rubinstein, 2012). Later throughout more developmental stages, parents may begin to notice short stature. Once the child begins schooling, the symptoms become slightly more obvious, demonstrating slow development of cognitive skills.
Once a child begins to perform tasks such as drawing, coloring, and using scissors, teachers and parents will begin to notice slow development of motor skills accompanied by low muscle tone (Morelli, 2012). These symptoms are also a bit more noticeable because due to RTS, the thumbs and toes on an affected child will broaden beyond normal size, complicating everyday tasks. This will severely limit to what extent a child suffering from RTS will be able to perform in the classroom. Rubenstein-Taybi Syndrome is not inherited by the parents or caused by anything the parents did or did not do while pregnant.
Most cases are caused by a single mutation in one gene. Rubenstein-Taybi Syndrome almost always occurs in cases where there is no family history of Rubenstein-Taybi Syndrome showing that family history and heredity is not a factor in contracting Rubenstein-Taybi syndrome. Most cases are sporadic and likely due to a new genetic defect that occurs while the baby grows in the womb, which was not passed on by either parent (Morelli, 2012). Consequently, parents with a child with a new mutation generally do not have an increased risk of having another child with the disorder.
However, the new genetic mutation will be hereditary and an adult with this mutation risks passing on the mutated gene to his/her children. However, it is unusual for people with the syndrome to become parents. There is no specific treatment for RTS that has been discovered as of yet. Because the disease is genetic, it is impossible for doctors to pinpoint just one area of the body to treat, especially because the disease comes with so many other symptoms. This however, does not mean that modern medical science cannot ease the way of life for a person with RTS.
Surgery to repair the bones in the thumbs or toes can sometimes improve grasp or relieve discomfort (Morelli, 2012). With all being said, it is incredible to imagine the difficulty that a student suffering with RTS may face in the classroom. A 1977 case study by Goots and Liemohn compared three children (aged seven to ten) with the syndrome to 15 counterparts with mixed mental retardation (Galera & Taupiac, 2009). In the study, it was found that children with RTS were friendly and more readily social. In addition, the students with RTS were more emotional and excitable.
Nightmares were seen more frequently, and the students were more likely to pout. Demonstrating lack of focus in the classroom, the students affected by RTS had short attention ps. Important in development at these ages, the students with RTS faced more difficulties in planning motor acts (Galera & Taupiac, 2009). Speech problems are present in a large percentage of students. Most individuals have speech delay, but others also have articulation problems. It is not unusual as well, to discover that some students with RTS use sign language as their primary form of communication.
Unfortunately for students with RTS, they often times confused with autistic students. References Galera, C. , & Taupiac,, E. (2009). Socio-Behavioral Characteristics of Children with Rubinstein-Taybi Syndrome [Abstract]. Journal of Autism & Developmental Disorders, 39(9), 1252-1260. doi: 10. 1007/s10803-009-0733-4 Morelli, J. G. (2007). Disorders of the Nails. In Nelson Textbook of Pediatrics (18th ed. , p. Chap 662). Phildelphia, PA: Saunders Elsevier. Rubinstein-Taybi Syndrome. (2012, February 27). Genetics Home Reference. Retrieved March 6, 2012, from http://ghr. nlm. nih. gov/condition/rubinstein-taybi-syndrome

Rubenstein-Taybi Syndrome Research Paper

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Cushing’s Syndrome

Cushing’s Syndrome.
Cushing’s Syndrome is a hormone disorder caused by the body tissues being exposed to high levels of the hormone cortisol for a long period of time. The disease is commonly caused by taking corticosteroid medicine in high doses over an extended period of time. The condition can also be caused by the body’s excess production of cortisol due to an overactive adrenal gland. It is a rare disease that mostly affects adults between the ages of 20 to 50. Females are more likely to get the disease than males due to an adrenal or pituitary tumor. Cushing’s Syndrome signs and symptoms include progressive obesity and skin changes.
There is rapid gain in the upper body fat deposit along the collar bone and the back of the neck which is often called “buffalo humps” and a rounded face which is referred to as “moon face”. The skin stretches causing pink or purple stretch marks along the stomach, thighs, breasts, and arms. A woman with the syndrome could experience excess body hair growth on their face, neck, chest, stomach, and thighs. It could cause their menstrual cycle to become irregular or stop. A man with the syndrome could experience decreased fertility and erectile dysfunction.
Other signs and symptoms include excess sweating, fatigue, muscle weakness, headaches, high blood pressure, thinning and fragility of the skin causing it to bruise easily and heal poorly. Other symptoms also include dryness of the skin, acne, weakened bones, cognitive difficulties, and high blood sugar which may lead to diabetes. Cushing’s Syndrome can also cause loss of emotional control which could lead to depression, anxiety, and irritability. The adrenal gland of the endocrine system produces a number of hormones, including cortisol.

Cortisol plays a number of roles throughout the body. It helps with regulating the body’s blood pressure, which keeps the cardiovascular system functioning normal. It helps to react to stress by converting proteins, carbohydrates, and fats into usable energy. The condition can be caused by medication such as prednisone that has the same effects as the cortisol that is produced in the body. A doctor may prescribe this type medicine to patients with inflammatory disease such as asthma, lupus, rheumatoid arthritis, or to prevent the body from rejecting a transplanted organ.
The treatment of these conditions often requires higher amounts of cortisol than the body normally needs in a day. The condition can be caused by your own body producing excess cortisol. This could occur from the excess production of one or both of the adrenal glands of the adrenocorticotropic hormone (ACTH) which regulates production of cortisol. A benign tumor of the pituitary gland can cause secretion of an excess amount of ACTH, which will, in return, stimulate the adrenal gland to make more cortisol than the body needs.
As mentioned previously, the condition occurs more often in women. Urine and blood lab tests are performed to measure the hormone levels in the urine and blood. These tests will show if the body is producing an excessive amount of cortisol. Saliva tests are also used by analyzing cortisol levels in salvia collected at night. Normally, cortisol levels rise and fall throughout the day, but levels in people without Cushing’s Syndrome will drop considerably in the evening. Imaging tests such as CT or MRI scans can detect abnormalities such as tumors in the pituitary and/or adrenal glands.
All of these tests can help a doctor diagnose Cushing’s Syndrome and rule out other medical conditions. The treatment for Cushing’s Syndrome depends on what caused the cortisol to be high in the body. The treatment should be designed to lower the high level of cortisol in the body. If the disease was caused by long term exposure to corticosteroids, then the treatment would be reducing the use of corticosteroid. For patients with asthma, arthritis, or other conditions that require medication to manage their illness, doctors can prescribe noncorticosteroid drugs.
Surgery is recommended if the disease is caused by a tumor that is present in the pituitary gland, adrenal glands, lungs, or pancreas. If surgery does not remove the tumor completely, radiation therapy is used in conjunction with the operation. Medications such as Nizoral, Lysodren, and Metopirone are prescribed to control production of cortisol when the surgery or radiation therapy doesn’t work. The length of recovery depends on the severity and cause of the Cushing’s Syndrome. Patients should be advised to increase their daily activities slowly due to weakened muscles.
They need to be sure that they are eating sensibly and getting enough calcium and Vitamin D to help strengthen their bones. They need to monitor their mental health because depression can develop due to being overwhelmed or having difficulty coping with recovery. For aches and pains; the patient can take hot baths and do low impact exercises such as water aerobics. For patient recovery from cognitive difficulties, they can do crossword puzzles or math problems to exercise their brain and help to improve their brain function.

Cushing’s Syndrome

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Baby Bottle Syndrome

Baby Bottle Syndrome.
Baby-Bottle Syndrome Putting an infant to bed with a bottle can result in aspiration or decay of all the upper teeth and the lower posterior teeth (Nainar & Mohummed, 2004); (Fig. 28. 21). Decay occurs because while an infant sleeps, liquid from the propped bottle continuously soaks the upper front teeth and lower back teeth (the lower front teeth are protected by the tongue). The problem, called baby-bottle syndrome, is most serious when the bottle is filled with sugar water, formula, milk, or fruit juice. The carbohydrate in these solutions ferments to organic acids that demineralize the tooth enamel until it decays.
To prevent this problem, advise parents never to put their baby to bed with a bottle. If parents insist a bottle is necessary to allow a baby to fall asleep, encourage them to fill it with water and use a nipple with a smaller hole to prevent the baby from receiving a large amount of fluid. If the baby refuses to drink anything but milk, the parents might dilute the milk with water more and more each night until the bottle is down to water only. | | |FIGURE 28. 21 Baby-bottle syndrome. Notice the extensive decay in the upper teeth. (K. L.
Boyd, DDS/Custom Medical Stock Photo. ) | Obesity in Infants Obesity in infants is defined as a weight greater than the 90th to 95th percentile on a standardized height/weight chart. Obesity occurs when there is an increase in the number of fat cells due to excessive calorie intake. Preventing obesity in infants is important because the extra fat cells formed at this time are likely to remain throughout childhood and even into adulthood. If a child becomes obese because of overingesting milk, iron-deficiency anemia may also be present because of the low iron content of both breast and commercial milk.

Once infant obesity begins, it is difficult to reverse, so prevention is the key (Benton, 2004). Overfeeding in infancy often occurs because parents were taught to eat everything on their plate, and they continue to instill this concept in their children. This appears to be the case most often with formula-fed infants whose parents urge them to empty their bottle or finish a cereal serving. It can occur any time parents automatically feed an infant when the child cries, rather than investigating what the cry might really mean. As a general rule, an infant should take no more than 32 oz of formula daily.
When solid food is introduced, a bottle of water can be substituted for formula at one feeding. Nonfat milk should not be given because it contains so little fat that essential fatty acid requirements may not be sufficient to ensure cell growth. Another way to help prevent obesity is to add a source of fiber, such as whole-grain cereal and raw fruit, to an infant’s diet. These prolong the stomach-emptying time, so they can help reduce food intake. Caution parents about giving obese infants foods with high amounts of refined sugars, such as pudding, cake, cookies, and candy.
Encourage parents to learn more about balanced nutrition and to provide this for their entire family. Care of Teeth It is well accepted that exposing developing teeth to fluoride is one of the most effective ways to promote healthy tooth formation and prevent tooth decay. The most important time for children to receive fluoride is between 6 months and 12 years of age. A water level of 0. 6 ppm fluoride is recommended because this is the level that protects tooth enamel yet does not lead to staining of teeth.
In communities where the water supply does not provide enough fluoride, the use of an oral fluoride supplement beginning at 6 months or the use of fluoride toothpaste or rinses after tooth eruption is recommended (AAP, 2001). P. 849 Teach parents to ask about the presence of fluoride in the drinking water in their community and help them to determine what, if any, supplementation is necessary. Breast-fed infants do not receive a great deal of fluoride from breast milk, so it may be recommended they be given fluoride drops once a day.
Teach parents to begin “brushing” even before teeth erupt by rubbing a soft washcloth over the gum pads. This eliminates plaque and reduces the presence of bacteria, creating a clean environment for the arrival of the first teeth. Once teeth erupt, all surfaces should be brushed with a soft brush or washcloth once or twice a day. Children lack the coordination to brush effectively until they are school-age, so parents must be responsible for this activity well past infancy. Toothpaste is not necessary for an infant, because it is the scrubbing that removes the plaque.

Baby Bottle Syndrome

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Compartment Syndrome

Compartment Syndrome.
Balancing Change Everyone experiences drastic changes or problems in their lives, and the ones who can react and find solutions to them will most likely end up conquering them. For some, it can take a long time to adjust, while others can come out on top quicker. It was a normal feeling Friday when I woke up on January 26th, 2007, but little did I know this would be the biggest challenge that I have ever had to face. “Ring…. ring….. ring,” the school bell rang deafeningly through the gymnasium.
It was first period, and the first class on my agenda for the day was my personal favorite, “P. E. ”, short for Physical Education. The class started out with our muscle-loosening stretches, and then moved on to one of my all-time favorite sports, basketball. The sparkling, brand new “Kobe Bryant 8’s” were a necessity for my feet in order to play. As I was tying the knots to begin, my best friend Ryan Decker glided swiftly into class with his “Heely’s”, which are shoes made with a wheel incorporated into the sole of the shoe. What did I do, when I first spotted them?
I asked him if I could try them on and roll around the gymnasium, because the slick floor provides a perfect surface for rolling around on. As I was rolling around, a basketball rolled in between my feet. I stared at it, and thought about it for a couple seconds. I thought to myself, “How cool would it be to roll from one side to the other, then shoot a layup right into the basket? ” Step by step, glide by glide, I was gaining speed. “BOOM! ” Before I could even comprehend what happened, I glared down at a surging pain that vibrated through my whole body, mainly sourcing from my left ankle.

My ankle was completely turned backwards. I frantically yelled out to my instructor, “MY ANKLE IS BROKEN! ” As he sprinted over to the other side of the gymnasium where I was laying in agony, I could see an audience starting to gather. He informed me that the ambulance was on its way and that my mother had been notified. Five minutes later, the ambulance arrived to my side. Before I knew it, I was placed into the ambulance, and I was on my way to seek urgent medical attention. Within four hours, I went through multiple x-rays, took a bunch of ain-killers, and a vibrant green colored cast was placed onto the lower half of my leg. Unfortunately enough, I had suffered a double break through my tibia, which is the second biggest bone in the human body, next to the femur. I thought to myself about all the consequences this would cause and how it would interfere with my everyday life. After a long ride home with my mother, I finally saw my house in the distance; I was home. With my leg still screaming with pain, I wondered why the pain was still so severe, even with the help of the pain killers.
I kept on repeating to my parents that I was still in excruciating pain. The pain was so unbearable that I couldn’t keep my mind off of it. This continued on for a couple days, but then something went terribly wrong. I tried to wiggle my toes to see if my movement was still there, but it wasn’t. Over and over again, I kept trying to move them and then I came to realize all of the movement in my foot was gone. I finally communicated to my parents that there was really something bad going on and that I needed to get rushed back to the hospital for a checkup.
After impatiently waiting in the waiting room for about an hour, I the doctor finally arrived to escort the family and I to the testing room. Then the worst words, that I will never forget came out of her mouth. “Robert……I made a mistake when I diagnosed you with a broken ankle…you have suffered from a condition called compartment syndrome. ” “Compartment syndrome is a limb threatening and life threatening condition, defined as the compression of nerves, blood vessels, and muscle inside a closed space (compartment[->0]) within the body.
This leads to tissue death from lack of oxygenation due to the blood vessels being compressed by the raised pressure within the compartment” (PubMed). All of a sudden, the doctor said I needed to be placed into surgery immediately before the condition worsened. I kept thinking about my future in school, sports, and most importantly my health. My education was in path to become a big failure, sports was not going to be a significant part of my life anymore, and hopefully my leg was still going to be attached to my body by the end of this.
After a successful surgery of putting in screws through my thick tibia bone, adding new tendons from a cadaver, and fixing it cosmetically, I finally woke up from the anesthesia. Movements with my ankle hurt like hell, but I didn’t even seem to care because I was able to regain movement and at least half of my feeling back. Eight weeks passed by, and I was finally able to start my physical therapy training to try and overcome this beast of an incident. The physical therapist first instructed me to walk down the hallway on about fifty percent of my weight.
As I was taking my second step I heard and felt a click in my ankle. The stitches holding my tendons together into place ripped through them like a soft cheese. I again was not able to move any part to my foot and ankle. I was back to square one once again. I was not physically and mentally prepared for something this bad to happen. I was going to have to go under the knife once more to fix this mess of an injury. This same instance of ripping through the cadaver’s tendon in my ankle happened five more times before I was fully healed. But what does fully healed mean?
Fully healed to me, meant nothing because of everything I went through to get to this point. No student should have to miss 3 months of school in one school year and have to be strayed from any scholastic activities for that long. No athlete should have to miss a whole season and championship run because of an injury. Lastly no human being should have to worry about their health and their chance of living at the age of fifteen. At the end of this challenge, I had to go through seven surgeries, when really it should’ve only taken about two.
Because the doctor never tested my ankle for compartment syndrome, I had to suffer. What did suffering do to me in the long run? It turned me into who I am today. A young man who feels like he can make his was through any adversity, problems, or change. When something bad happens to yourself, you are given two choices: either to react in a manner aiming to better yourself from the situation, or to grieve and stay emotionally broken. Always keep your head up, and never think the worst because it can always get better with the right attitude.
I am now right back on track with my education, and the ankle feels better than ever. Never again, will I ever put on another pair of “Heely’s” in my life. The art of being able to balance change is something that I believe has transformed me into the person I am today and the person I am going to be. Works Cited: Board, A. D. A. M. Editorial. Compartment Syndrome. U. S. National Library of Medicine, 18 Nov. 0000. Web. 09 Oct. 2012. . [->0] – http://en. wikipedia. org/wiki/Compartment_(anatomy)

Compartment Syndrome

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Joint Problems Patellofemoral Pain Syndrome Health And Social Care Essay

Joint Problems Patellofemoral Pain Syndrome Health And Social Care Essay.

Patellofemoral articulation jobs are the most common overuse hurt of the lower appendage, and altered femoral or hep rotary motion may plays a major function in patellofemoral hurting
Patellofemoral hurting syndrome ( PFPS ) is the 2nd most common musculoskeletal ailment presented to physical therapists ( Witvrouw et al, 1996. Hilyard, 1990 ) . Studies has shown Patello Femoral Pain Syndrome to be the most common individual diagnosing among smugglers and in athleticss medical specialty centres. Eleven per centum of musculoskeletal ailments in the office scenes are caused by anterior articulatio genus hurting ( which most normally consequences from PFPS, constitutes 16-25 % of all hurts in smugglers ) . The term PFPS is frequently used interchangeably with “ anterior articulatio genus hurting ” or “ smuggler ‘s articulatio genus ” .
Patellofemoral hurting syndrome can be defined as retropatellar or peripatellar hurting ensuing from physical and biomechanical alterations in the patellofemoral articulation. It should be distinguished from chondromalacia, which is existent fraying and harm to the underlying patellar gristle.

Patients with patellofemoral hurting syndrome have anterior articulatio genus hurting that typically occurs with activity and frequently worsens when they are falling stairss or hills. It can besides be exacerbated by activities such as go uping stepss, crouching, kneeling, drawn-out posing ( Doucette and Goble, 1992 ) . The oncoming of the
symptom is normally insidious ( Arroll et al, 1997: Hilyard, 1990 ) . One or both articulatio genuss can be affected.
Many factors are involved in complex interactions that influence the patellofemoral articulation and the exact aetiology and pathophysiology of PFPS is frequently puzzling ( Fulkerson and Hungerford, 1990 ; Finestone et Al, 1993 ) . Many theories have been proposed to explicate the etiology of the patellofemoral hurting. These include mechanical, muscular and over use theories. There is consensus that malalignment and maltracking of the kneecap are major characteristics of PFPS ( Maclntyre and Robertson,1992: Gerrard, 1989 ) .
The patellar maltracking consequences in unnatural joint emphasis and subsequent articular gristle ware ( Powers: 1998 ) . Lateral trailing of the kneecap has been listed as a major subscriber to malalignment which consequences in unnatural joint compaction and later patellar hurting.
It is normally theorized that maltracking is the consequence of vastus medialis ( VM ) weakening comparative to the vastus lateralis ( VL ) , ensuing in sidelong trailing of kneecap ( Mc Conell, 1986 ) . Weak hip muscular structure is besides thought to lend to unnatural trailing of kneecap. Ireland et Al found that adult females with PFPS are 26 % weaker hip abduction and 36 % weaker in hip internal rotary motion compared
with healthy controls. Such failing may do an addition in both varus force vector at the articulatio genus a combination that may farther ease median trailing of kneecap.
Lower appendage malalignment ( caused by abnormalcies such as an increased standing ‘Q ‘ angle, pes planus or subtalar pronation ) frequently has been implicated as a cause of PFPS.
Most patients with PFPS respond favorably to conservative intercession. These include quadriceps beef uping, patellar tape, patellar brace, stretching, soft tissue mobilisation. With the most common intervention being quadriceps beef uping utilizing weight bearing and non weight bearing exercisings, weight bearing exercisings are more functional than non weight bearing exercisings because they require multijoint motion, easing a functional form of musculus enlisting and stimulate proprioceptors.
In an attempt to supply immediate decrease to trouble, Mc Conell proposed utilizing tape to modify patellar orientation and normalise patellar trailing. When handling patients with patellofemoral hurting who demonstrate deficiency of control of hip abduction and external rotary motion during weight bearing activities such as walking and falling stepss, one end may to be to optimise musculus map to command these gestures, as such motion can ensue in knee varus, an addition in dynamic
‘Q ‘ angle and greater median forces moving on the kneecap. Hence, it would look sensible to endeavor for optimum map of hip muscular structure.
1.2 BACKGROUND AND PURPOSE OF THE STUDY
Despite its prevalence, nevertheless the etiology and specific intervention of this hurting syndrome remain obscure and controversial. The premiss behind most intervention attacks is that Patellofemoral hurting syndromes is the consequence of malalignment and/or unnatural patellar trailing. Interventions are frequently focused locally and typically include quadriceps beef uping, patellar tape, patellar brace and soft tissue mobilisation. Based on the old researches, we theorized that the exercisings stressing neuromuscular control of both the quadriceps and hip median rotators may profit patients diagnosed with PFPS. Therefore, the intent of this survey was to look into the effects of hip median rotators and quadriceps beef uping plan in patients with patellofemoral hurting syndrome.
Need AND SIGNIFICANCE OF STUDY:
Need of the survey:
To cut down hurting
To better scope of gesture
To better functional activity
Aims:
To find the effectivity of median rotator musle and quadriceps beef uping in patellofemoral hurting
To find the effectivity of quadriceps beef uping in patellofemoral hurting
To compare the effectivity of quadriceps beef uping and median rotator musculus beef uping exercising in patellofemoral hurting
1.3 HYPOTHESIS
The void hypothesis for this survey could be stated as “ There Is No Significant Difference In Reduction Of Pain between the group having Hip Medial Rotator and Quadriceps Muscle Strengthening when compared with Quadriceps Muscle Strengthening entirely in Patients With Patellofemoral Pain ” .
REVIEW OF LITERATURE
Cibulka MT, Threlkeld-Watkins J. , 2005 has reported that patellofemoral hurting is the commonest of all the overexploitation hurts of the lower limb. Major cause for this is considered to be altered femoral rotary motion.
Powers CM. , 2003 has demonstrated that patellar maltracking and malalignment are the commonest triggering factors for kneecap femoral hurting.
Mascal CL, Landel R, Powers C 2003 has concluded in their survey that musces of hip, bole and pelvic girdle are affected in patellofemoral hurting syndrome and hence intercessions directed towards these muscular structure should be included in the rehabilitation protocol.
Bellamy N, Buchanan WW, Goldsmith CH, Campbell J, Stitt LW 1988 has published a survey on WOMAC graduated table reasoning that WOMAC is the most dependable and valid graduated table for measuring arthritis.
Braten M, Terjesen T, Rossvoll I 1992 has demonstrated that ultrasound analysis of hip in anterior articulatio genus hurting reveals femoral rotary motion in most of the patients.
i?? Sameer A.Dixit, M.D. , et al Management of patellofemoral hurting syndrome shown that physical therapy is effectual in handling PFPS.
i?? La Brier K, O ‘ Neill D.B, Patellofemoral syndrome, current constructs. This survey indicate that patellofemoral hurting syndrome is normally treated cautiously, surveies indicate that 60 % to 89 % of articulatio genuss will react favorably to conservative intervention. The exercising plan include Iliotibial set, hamstring and gastrocnemius stretching, progressive opposition straight leg elevation and hip adduction beef uping performed 2 times/ twenty-four hours until symptoms subside and the 3 times /week, thenceforth.
i?? Heintjes, Berger MY, Bierma- Zeinstra SM, Exercise therapy for patellofemoral hurting syndrome stated that the exercising therapy is more effectual in handling PFPS. There is strong grounds that unfastened and closed kinetic concatenation exercising are every bit effectual.
i?? Hudson Z, Daruthy E. Iliotibial set stringency and patellofemoral hurting syndrome. A instance – control survey show that the topics showing with PFPS do hold a tighter ITB.
i?? Fagan V, Delahunt E, Patellofemoral pain syndrome- a reappraisal of the associated neuromuscular shortages and current intervention options stated that “ Physiotherapy intervention programmes look to be an efficacious method of bettering quads instability.
i?? Power et, Al, ( 1997 ) , patient performed free walking, fast walking, go uping and falling walking with and without patellar taping. Taping determined patient ‘s hurting reduced ( VAS ) 50 % during exacerbating activity.
i?? Ernst GP, Kawaguchi. J, Saliba E. Effect of Patellar Taping on articulatio genus dynamicss of patients with patellofemoral hurting syndrome, suggests that patellar taping compared with no tape may better the articulatio genus extensor minute and power during weight bearing activities such as sidelong measure – up exercising and perpendicular leap.
i?? Cristina mare Nunes cabral, Amellia Pasqual Marques, Effect of a closed kinetic concatenation exercising protocol on patellofemoral syndrome rehabilitation. The consequences of T he study allow the suggestion that the proposed quadriceps femoris beef uping exercisings with ROM control should be prescribed for PFPS patients since they improve knee functional degree.
i?? Avraham.F, Aviv.S et al. , The efficaciousness of intervention of different intercession plans for patellofemoral hurting syndrome. The survey with a sum of 30 back-to-back patients ( average age 35 old ages ) diagnosed with PFPS indiscriminately allocated into 3 groups. Group I – Conventional Rehabilitation plan included quadriceps beef uping and TENS, Group II- Hip oriented rehabilitation plan included stretching,
hip external rotator strengthening and TENS. Group III-A combination of 2 plans.
At terminal of test all groups show important betterment in VAS and PFJES ( P & lt ; 0.0001 ) ; these betterment did non vary significantly between the 3 groups. All the groups show a similar good consequence.
i?? Tyler TF, Nicholas SJ, Mullaney MJ. The function of hip musculus map in the intervention of patellofemoral hurting syndrome. This survey concluded that betterments in hip flexure strength combined with increased iliotibial set and iliopsoas flexibleness were associated with first-class consequences in patients with patellofemoral hurting syndrome.
i?? Harmonizing to Muir KR ( 1999 ) . a individual plan of place quadriceps can significantly better ego reported articulatio genus hurting and map.
i?? Cheng GL et Al in their survey conducted for four hebdomads intervention period, concluded that both TENS and isometric groups had important decrease in articulatio genus hurting.
i?? Sheila O ‘ Reilly made a survey on 192 work forces and adult females with articulatio genus hurting. They were enrolled in a plan consisting of isometric and isosmotic exercisings of the quadriceps or thigh, utilizing a opposition set and they had important lessening in hurting ( 22.5 % ) and betterment in physical map ( 17.4 % ) . She besides stated that beef uping musculuss around an creaky articulation could back up the joint and cut down hurting.
i?? Lam PL, NG QY, Activation of the quadriceps musculus during semi crouching with different hip and knee place in patients with anterior articulatio genus hurting, the survey shows that there was comparatively more activation of vastus medialis oblique than vastus lateralis at 40A° of semi knee bend with hip medially rotated by 30A° .
i?? Herrington L. AL – Sherhi.A, A controlled test of weight bearing versus non weight bearing exercisings for patellofemoral hurting. This survey demonstrates that both weight – bearing and non weight bearing exercisings can significantly better subjective and clinical results in patients with PFPS.
i?? Ng GY, Cheng JM, The effects of patellar taping on hurting and neuromuscular public presentation in topics with patellofemoral hurting syndrome. This survey states that there was a important lessening in anterior articulatio genus hurting ( P & lt ; 0.001 ) and vastus medialis obliques to vastus lateralis activity ratio ( P – 0.05 ) during individual legged standing after patellar tape.
i?? Mark overington, BHSc ( Physio ) , Damain Gooddard, BhSc ( Physio ) . , A Critical assessment and literature review on the consequence of patellar tape, is patellar taping effectual in the patellofemoral hurting syndrome? This critical analysis has shown that patellar taping lessenings pain in the short term, may be utile as an adjunct to physiotherapy in long term
i?? T.K. Amell, J.P. Stothart, S. Kumar, The effectivity of functional pes orthoses as a intervention for patellofemoral emphasis syndrome: A clients position. The consequences shows that orthotic usage is believed to be effectual in commanding the symptoms of PFPS.
i?? Michael T. Gross, PT. Ph.D. , Jody L. Foxworth, PT, MS, OCS, The Role of pes orthoses as an intercession for patellofemoral hurting. The mechanism for pes orthoses holding a positive consequence on hurting and map for these patients.
i?? Dr. Robert Topp assessed the hurting, map, abilities, knee joint proprioception, pace features and quadriceps strength of 135 participants utilizing randomized isometric strength preparation group and a dynamic strength preparation group for 16 hebdomad regimen and concluded that regular strength preparation could detain the oncoming of this painful disease and demand for surgery
i?? Van Berr et Al, ( 1999 ) found that aerophilic exercising was more effectual than opposition exercising in cut downing hurting. There was modest betterment in disablement degree for patients randomized to aerobic exercising.
i?? Michelle C. Boilig, MS, ATC. , et al. , Outcomes of a weight bearing rehabilitation plan for patients diagnosed with patellofemoral hurting syndrome. Subjects diagnosed with PFPS responded favorably and rapidly to a curative exercising plan that incorporated quadriceps and his muscular structure strengthening.
i?? Catherine L. Mascal PT, B.Sc. , Robert Landel, DPT, OSC, Christopher power, PT, Ph..D. Management of Patellofemoral hurting Targeting the Hip, Pelvis and Trunk Muscle map: instance study. This instance study present 2 patients with PFP who demonstrated unnatural kinematics at the hip and who respond favourably to an exercising plan specifically aiming to Hip, Pelvis and trunk muscular structure.
3.MATERIALS AND METHODOLOGY
3.1 METHODOLOGY
3.1.1.STUDY Design
The survey was conducted in the format of experimental pre-test, station trial survey design.
3.1.2STUDY Setting
The survey was conducted in the section of physical medical specialty and rehabilitation, Ramakrishna Hospital, Coimbatore-641044 under the supervising of usher incharge, College Of Physiotherapy, SRIPMS, Coimbatore.
3.1.3SAMPLING
20 Subject who fulfilled the undermentioned criterias were selected through simple random sampling and assigned to two groups of 10 each.
CRITERIA FOR SAMPLE SELECTION.
I ) Inclusion standards
i?? Age between 25-35 old ages
i?? Both males and females
i?? Unilateral patellofemoral hurting syndrome and median rotator musculus weekness.
i?? Anterior or retropatellar articulatio genus hurting reported during at least two of the undermentioned activities: rise and falling step, skiping and running, crouching, kneeling, and prolonged posing.
i?? Insidious oncoming of symptoms non related to injuries.
i?? Pain with compaction of kneecap.
i?? Pain on tactual exploration of patellar aspects.
two ) Exclusion Criteria
Symptoms nowadays for less than two months
No history of old articulatio genus hurting
Metallic element implants
Fleshiness
Diabetess
Peripheral vascular disease
Self reported clinical grounds of other articulatio genus pathology. Such as intra articular pathology, peripatellar tendonitis or bursitis, fold, disruptions or subluxations etc.
Current important hurt impacting other lower appendage articulations.
Subjects with any of the above said conditions were excluded from survey.
Procedure:
1. Group A:
Subjects were treated with Hip median rotator and quadriceps beef uping exercisings and stretching.
2. Group B:
Subjects were treated with lone quadriceps beef uping exercisings and stretching.
Both group received the place programme of stretching and beef uping exercisings ( SEE APPENDIX – Four )
STUDY DURATION
This survey is proposed to be carried out for the period of 6 months
TREATMENT DURATION
Group A:
5 sets of 12 repeats per twenty-four hours 3 yearss per hebdomad for 4 hebdomads
Group B:
5 sets of 12 repeats per twenty-four hours 3 yearss per hebdomad for 4 hebdomads
Parameters
Subjective hurting strength during activities of day-to-day life measured with ocular parallel graduated table ( VAS ) .
Functional activities measured with western Lake Ontario andmcmaster universities osteoarthritis index ( womac )
3.2MATERIALS USED
Orthopedic rating chart
Thera set
Strengthening sofa
Inch tape
3.3 Statistical Tool
The consequences of the survey were analysed utilizing independent ‘t ‘ trial
T =
S =
= Mean difference of the first group
= Mean difference of the 2nd group
= Number of samples in first group
= Number of samples in 2nd group
S = Combined criterion divergence
TREATMENT TECHNIQUES
Exercise FOR PATELLOFEMORAL PAIN SYNDROME
Strengthening Exercises:
1 ] Hip internal rotators beef uping
this exercising is performed with the patient standing in the exercising machine. Initially 5 sets of 12 repeats get downing with 9kg is done and later opposition is increased harmonizing to musculus weariness and hurting.
2 ] Quadriceps Strengthening:
A ] Isometricss:
Position yourself as shown above. Keep your right leg straight for 10-20 seconds and so loosen up. Make the exercisings 5-10 times.
B ] Straight Leg Raising:
Position yourself as shown above. Raise your right leg several inches and keep it up for 5-10 seconds. Then lower your leg to the floor easy over a few seconds. Do the exercisings 5-10 times.
3 ] Partial Knee bends:
Stand with pess, shoulder width apart and toes somewhat turned out. Bend articulatio genuss from traveling in forepart toes. Squat every bit low as tolerable, intermission at lowest deepness and raise to get downing place. It can besides be done with back support on wall and with ball between 2 articulatio genuss.
4 ] Step Up:
Stand sideways with involved leg next to 3-6 ” measure. Place involved pes on measure and easy raise organic structure weight with involved leg. Slowly lower organic structure back to get down place gently touching heel on
land, so repetition by easy raising organic structure with involved leg. Repeat as by increasing repeat. Increase measure 2-3 ” with repeat.
Stretching Exercise
1a ) Iliotibial Band Buttock Stretch: ( Right side ) .
Position yourself as shown in the image. Writhe your bole to the right and utilize your left arm to “ force ” your right leg. You should experience the stretch in your right thigh. ( Hold the stretch for 10 to 20 seconds. Do the exercising 5 to 10 times ) .
B ) Iliotibial Band Stretch: ( Left Side )
Position yourself as shown below, with your right leg crossed in forepart of your left leg. Keep your custodies together and travel them toward the floor. You should experience a stretch in the outer portion of your left thigh. ( Hold the stretch for 10 to 20 seconds. Do the exercising 5 to 10 times. )
2 ) . Hamstrings stretch:
Liing in back and back uping thigh behind articulatio genus, easy straighten articulatio genus until a stretch is felt in the dorsum of the thigh. Keep it for 5 to 10 seconds. Repeat it for 5 to 10 times. The thigh may besides be supported on a wall.
3 ) Quadriceps Stretch:
Position with one manus on the wall and the other on the pes of the side to be stretched and the articulatio genus is flexed. Keep it for 5 to 10 seconds. Repeat it for 5 to 10 times. Can be performed with hip flexure and extension.
4 ) Calf Stretch:
Position against a wall with heel on the land to experience back of the leg stretch. Keep for 10 to 20 seconds. Do the exercisings 6 to 10 times.
5 ) Hip And Buttock Stretch: ( Left Side )
Position left over right leg and manus is placed over left articulatio genus draw the articulatio genus somewhat towards the patient while sitting up directly. Keep the place for 20 seconds and so rest for several seconds. Do the exercising for 6 times.
6 ] Hip Adductor Stretch:
Position in supine prevarication, with hip and articulatio genus flexure, and inquire the patient to kidnap the leg until the stretch felt. Keep it for 10-20 seconds, repetition it for 5-10 times.
7 ] Hip external rotators Stretch:
Gentle stretching of the hip in the way of median rotary motion is done with the patient in prone prevarication. Stretching is done with the hip in impersonal and knee flexed to 90 grade. The stretch force is held for 30 seconds and repeated for 3 times.
4. DATA PRESENTATION AND ANALYSIS
GROUP – A ( VAS )
S.No
PRE – Trial
POST -TEST
Difference
7
2
5
6
1
5
5
2
3
8
3
5
4
1
3
5
1
4
7
2
5
8
3
5
5
1
4
6
1
5
Mean
6.1
1.7
4.4
GROUP – B ( VAS )
S.No
PRE – Trial
POST -TEST
Difference
7
3
4
5
2
3
7
4
3
8
4
4
6
3
3
5
2
3
7
3
4
7
3
4
5
3
2
5
1
4
Mean
6.2
2.8
3.4
Vessel
Group
MEAN VALUE
CALULATED “ T ” Value
Table “ T ” Value
PRE – Trial
POST -TEST
South dakota
A
6.1
1.7
1.46
2.888
0.01
Bacillus
6.2
2.8
1.33
GROUP – A ( WOMAC )
S.No
PRE – Trial
POST -TEST
Difference
35
27
8
37
27
10
41
31
10
39
30
9
42
33
9
35
28
7
43
35
8
40
31
11
35
26
9
38
31
7
Mean
38.6
29.9
8.8
GROUP – B ( WOMAC )
S.No
PRE – Trial
POST -TEST
Difference
38
29
9
40
32
8
38
31
7
40
33
7
42
35
7
36
30
6
40
31
9
30
22
8
35
28
7
40
34
6
Mean
37.9
30.5
7.4
WOMAC
Group
MEAN VALUE
CALWLATD “ T ” Value
Table “ T ” Value
PRE – Trial
POST -TEST
South dakota
A
38.6
29.9
1.32
2.606
0.05
Bacillus
37.9
30.5
1.07
Discussion
This survey was done to happen out the effectivity of hip median rotator and quadriceps musculus beef uping in patients with patello femoral hurting syndrome. Twenty patients who had PFPS for continuance of atleast two months participated in this survey. They were indiscriminately allocated to one of the two intervention groups. Group I received hep median rotator and quadriceps musculus beef uping plan and Group II received merely Knee quadriceps musculus beef uping plan. Patients were evaluated after two months of intervention and all patients completed the survey.
The statistical analysis performed between Group I and Group II showed the undermentioned result. VAS mark showed the average betterment of 3.4 and 4.4 of hip median rotator and quadriceps musculus beef uping group severally.
The statistical analysis performed between Group I and Group II showed the undermentioned result. WOMAC mark showed the average betterment of 7.4 and 8.8 of median rotator and quadriceps musculus beef uping group severally.
The independent ‘t ‘ trial was performed to analyze the consequences. For VAS the deliberate ‘t ‘ value is 5.84 which is more than the table value of 2.101 in conformity to the degree of significance of 0.05, at 18 grades of freedom. The result is considered to be important prefering the rejection of void hypothesis.
For WOMAC the calculated’t ‘ value is 2.606 which is more than the table value 2.101. The result is considered to be important prefering the rejection of void hypothesis
Therefore, “ There is a important difference in decrease of hurting on utilizing hep median rotator and quadriceps musculus beef uping patients with PFPS.
The consequences showed important decrease in hurting degree with both rehabilitation plan but the hip median rotator and quadriceps musculus beef uping showed greater diagnostic recovery than the knee quadriceps beef uping. Hence, based on the ‘t ‘ value, it is clear that there is a important difference between two beef uping programmes.
A restriction of our survey is that merely one-sided patello fermoral hurting syndrome was taken for the survey.
Decision
Based on the consequences of our survey, it is clear that hip median rotator and quadriceps musculus beef uping howed greater diagnostic recovery than the knee quadriceps beef uping plan entirely. This suggests that the implicit in cause of patellofemoral hurting in certain persons may non be restricted to the patellofemoral articulation.
From this survey it is suggested that hip median rotator and quadriceps musculus strengthening is more good to patients with patellofemoral hurting syndrome.
Since it is a clip edge survey, survey with the larger sample size and long term follow- up can be done in hereafter.

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