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Angina Pectoris

Angina pectoris pain is a clinical syndrome causing pain or pressure in the centre of the chest. Usually exercise – sometimes acute anxiety & stress – brings on angina pectoris pain. This is because angina pectoris pain can accompany myocardial ischaemia and coronary artery disease. Angina pain may be severe and felt also in arms and the jaw.

Neurologically, ischaemia (associated with angina pectoris pain) stimulates pain fibres which pass to the sympathetic ganglia between vertebra C7 and T4 (i.e. top of the upper back).

Epidemiology of Angina Pectoris Pain

Angina pectoris pain affects approximately 1% of the population. This is made up of about 726,000 men and around 393,000 women in the UK (British Heart Foundation). Angina pectoris pain affects people aged between 35 and 75 years. Incidence of angina pectoris pain increases with age.

Types of Angina Pectoris Pain

- Chronic Stable Angina
- Nocturnal Angina
- Unstable Angina
- Variant Angina (Prinzmetal’s)
- Decubitus Angina
- Syndrome X (angina)

The chest pain (associated with angina pectoris pain) can also be caused by cold wind, emotion, or digesting a heavy meal. Usually what happens is the muscles of the heart do not receive enough oxygen, via the blood, for the work they are doing. This may cause the patient to breathe more deeply, thus recruiting the accessory muscles of inspiration. All the respiratory muscles are located in the neck and thoracic regions.

Heart

Another reason for why the patient may be breathing deeply could be due to his history of heart attacks (associated with angina pectoris pain). After a heart attack, scar tissue will replace the dead myocardial tissue, which is not contractile. This means the remaining contractile tissue has to work harder to compensate for this loss of efficiency. As a result, there is a decrease of oxygen supply to the body, so the patient will try to breathe deeper to increase their oxygen supply. Again, they will do this by recruiting the accessory muscles of inspiration, which can fatigue thereby causing pain and hypertonia. This can also cause angina pain (or angina pectoris pain).

The heart can generate its own electrical impulses, which initiate contraction. The sino-atrial node (SAN) is like the natural pace maker of the heart. Waves of excitation spread right across both atria. If a heart were taken out of the body, it would beat at a very fast rate.

Cardiac referred pain radiates from substernal and left pectoral regions to the left shoulder and the medial aspect of the left upper limb.
The heart receives its nerve supply from the vagus nerve. The parasympathetic nerve supply decrease this rate and strength of contraction, similar to the gentle braking of a car travelling down a steep hill. The nerve supply of the pericardium is from phrenic nerves C3, 4, 5, vagus nerves and sympathetic trunks.

An enlarged heart can impinge on the phrenic nerve and left recurrent phalangeal nerve are its posterior relations. In this case, the patient may lose their voice! The right and left bronchi lie superoposteriorly to the heart, which can also be affected if the heart is enlarged.

The relations of the heart laterally are the lungs. Posteriorly there is the oesophagus, and anteriorly the posterior surface of the sternum and costal cartilage. The diagphragm and central tendon are inferior to the apex of the heart.

Patients with angina pectoris pain often present with muscular pain due to their posture. For example, every time they have an angina pectoris pain attack, they usually flex their thoracic region for comfort and relief. Similarly, tissue changes in an area after an operation can alter the posture.

Treatment for Angina Pectoris

Medication for angina pectoris pain includes sublingual nitroglycerin (placed or sprayed under the tongue for absorption through the oral mucosa), glycerin trinitrate and propanolol. Its purpose is to dilate the coronary arteries, increases blood flow to the heart and usually relieves angina pectoris pain.

Osteopathic treatment for angina pectoris pain will relax tight, hypertonic muscles. As mentioned above, there is a neurological link to vertebra from C7 to T4. Your Osteopath may help improve neurological flow in this area to help alleviate angina pectoris pain symptoms. Patients with heart conditions tend to be very anxious and stressed. People who have had a heart attack usually describe a “crushing” substernal pain (deep to the sternum) that does not disappear with rest.

Relaxation may prove very useful to reduce anxiety and/or stress e.g. with yoga, meditation, aromatherapy – especially during an attack of angina pectoris pain.

Stress can also cause lower back pain in some people. If you spend most of your day at a desk, it is important to ensure your ergonomics are correct to reduce stress.

Posted by Mr. Trishul Vadi (Principal Osteopath in West Wickham, Beckenham, Bromley & South East London) on Thursday, August 12th, 2010

Lower Back Pain

About Lower Back Pain

Lower back pain can affect anyone, but is very common is people aged 35-55. Back pain can be divided into three categories:
1) Acute lower back pain – lasting less than 6 weeks
2) Sub-acute lower back pain – lasting 6 weeks to 3 months
3) Chronic lower back pain – lasting more than 3 months

Click here to find out how your back works.

Causes Of Lower Back Pain

Lower back pain can be caused by several different structures. In a lot of cases low back pain is caused by several factors coming together, rather than just one tissue type being affected. Here are some specific causes of lower back pain:

- Muscle sprain
- Disc protrusion
- Prolapsed disc (a.k.a. slipped disc or herniated disc)
- Spinal stenosis
- Collapsed vertebra
- Intervertebral joint lesion

Lower back pain and back ache is on the rise. One of the reasons for this is we are spending more time sitting than ever before. Think about it. Someone who has an office or desk based job sits at work, sits to and from work, then sits at home. Our bodies are designed to move. In fact our bodies depend on movement to maintain health. The spinal discs and cartilage in our bodies have no blood supply. This means that they have a poorer rate of recovery. Every time we move, these discs and cartilage get squeezed which aids the excretion of waste products. When released, fresh fluid floods back in to hydrate and nourish the tissues. If this process does not occur efficiently and regularly, the long term effects will results in lower back pain.

Other causes of lower back pain can also present with the following symptoms:
- fever / high temperature
- swelling in low back area
- redness over low back area
- pain in the legs (particularly below the knees)
- numbness, weakness or tingling in leg(s) and/or buttock(s)
- incontinence (loss of bladder and/or bowel control)
If you suffer from any of these other symptoms then you must contact your Osteopath immediately!

“Red flags” of lower back pain are a cause for concern and you must contact your Osteopath urgently if any of the following ever apply to you:
- result of an injury (e.g. car accident, road traffic accident, whiplash)
- aged under 20 or over 55 years with lower back pain lasting more than a few days
- currently have, or had cancer in the past
- have HIV/AIDS
- long term steroid medication

Diganosis Of Lower Back Pain
Your Osteopath will ask you to accurately describe the symptoms of your lower back pain during the case history, followed by a thorough examination. Further tests may also be carried out, such as neurological, cardiovascular, lymphatic, respiratory examinations. If the Osteopath suspects there to be an underlying pathology causing your symptoms, they may refer you for tests such as X-rays, CT scans, MRI or blood tests.

Treatment
Once an accurate diagnosis of your low back pain is made treatment may begin. Osteopathic treatment for low back pain involves a range of articulation, manipulation, soft tissue massage and traction techniques.

However there are things that you can do to help when you are suffering from lower back pain:
- Keep active – staying as mobile as you can is important in ensuring your condition does not worsen. Only move in a pain-free range however.
- Take rest – In cases where any movement is causing extreme pain, rest is vital for your body to recover.
- Heat – Heat is good in cases where your low back pain is caused by muscle spasm.
- Ice – Ice applied locally brings down inflammation of muscles and joints. Note however if applied for too long, this can have a negative affect so please contact us for specific advice.

Surgery
Surgery is the last resort with regards to your low back pain. The Osteopath’s job is to delay the requirement for surgery as much as they can. However if surgery is required then Osteopathy can help both before and after surgical intervention.

Prevention
Regular appointments at The Osteocare Clinic help diagnose and treat low back pain before they worsen. Keeping active is vital in the prevention of lower back pain. However if you have a desk based job this can often prove quite difficult. Have a look at our blog post on Office Space on tips on how to improve your sitting posture. Reducing stress is also important in keeping healthy.

Links:
- Lower Back Pain
- Obesity & Lower Back Pain

Posted by Mr. Trishul Vadi (Principal Osteopath in West Wickham, Beckenham, Bromley & South East London) on Friday, August 6th, 2010

HIV-related loss of joint motion

Research Paper 2006: Measuring the effects of HIV-related distal symmetrical peripheral neuropathy on joint range of movement using the “prayer” sign.

Author: Trishul Vadi
Supervisor: Paul Blanchard

Acknowledgments

The author would like to thank the following people for their help and support in carrying out this undergraduate research study:
Paul Blanchard for supervising this study. Will Podmore and Claire Baron for their support and generosity at The British School of Osteopathy.

Abstract
Background As osteopaths we assess and treat joints with every patient. This is an area where there has been no previous research carried out, and therefore would be of great benefit to the profession.

Objective The aim of the study was investigate the affect of distal sensory peripheral neuropathies (DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY) on joint range of movement (RANGE OF MOVEMENT) in human immunodeficiency virus (HUMAN IMMUNODEFICIENCY VIRUS) positive patients by measuring the ability to actively extend the interphalangeal joints of the hand using the “prayer”sign.

Methods Twenty-four patients with HUMAN IMMUNODEFICIENCY VIRUS infection were recruited frange of movement the Royal Free Hospital.

Results There was no statistical difference between VPT mean data and “prayer” sign scores, using Spearman’s Rank Correlation Coefficient for statistical analysis.

Conclusions Results suggest there is no effect of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY on joint RANGE OF MOVEMENT in HUMAN IMMUNODEFICIENCY VIRUS patients. Further research using larger samples with more subjective information frange of movement participants need to be investigated.

Keywords: cheiroarthropathy, “prayer” sign, HUMAN IMMUNODEFICIENCY VIRUS-infection, Peripheral Neuropathy, limited joint mobility, interphalangeal joints, Vibration Perception Threshold.

Introduction

Osteopathy does not claim to treat conditions, but to treat people who may happen to have a certain condition. Osteopaths do not claim to cure a person of their disease, but to improve that person’s quality of life. This is of great importance in conditions such as Human immunodeficiency virus (HUMAN IMMUNODEFICIENCY VIRUS).

Peripheral neuropathy (PERIPHERAL NEUROPATHY) is the most common neurological complication of a HUMAN IMMUNODEFICIENCY VIRUS infection (Keswani et al 2002; Luciano et al 2003; Wulff et al 2000). Distal symmetrical peripheral neuropathy (DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY) is due to neuropathological damage by HUMAN IMMUNODEFICIENCY VIRUS infection. It was known to be a common neurological sign of Acquired Immunodeficiency Syndrange of movemente (AIDS) before HUMAN IMMUNODEFICIENCY VIRUS had been detected as the cause of the syndrange of movemente (Keswani et al 2002).

Clinical signs and symptoms of HUMAN IMMUNODEFICIENCY VIRUS-related DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY are distal and symmetrical numbness, paraesthesias, and dysaesthesias; decreased joint range of movement; reduced/absent ankle reflexes; reduced pain and temperature sensation in glove and stocking distribution; increased vibratory threshold (Wulff et al 2000). Motor examination shows no abnormalities. It usually affects 30% of patients with a CD4 cell count equal to or below 200/µl. (Brew 2003).

PERIPHERAL NEUROPATHY in diabetes mellitus (DIABETES MELLITUS) is very common, affecting more than 50% of patients. “Small fibers are often involved early and predisposed the feet to injuries and subsequent diabetic ulceration” (Al-Shekhlee et al 2002 pp.240).

There are some key similarities between DIABETES MELLITUS and HUMAN IMMUNODEFICIENCY VIRUS. Neuropathies of both conditions affect the small and large fibres (Al-Shekhlee et al 2002). Type 1 DIABETES MELLITUS and HUMAN IMMUNODEFICIENCY VIRUS patients have limited joint mobility (LIMITED JOINT MOBILITY) due to neuropathy (Duffin et al 1999).

LIMITED JOINT MOBILITY is also known as cheiroarthropathy, “frange of movement the Greek cheiro for hand” (Aljahnlan et al 1999). This is a reduction in the flexibility of the joint. “Flexibility is the angle of width in the articulation movement, the ability to move the body and its parts (involved) to reach their maximum limits without causing any damage” (Komatsu et al 2004 pp.1).

It is caused by the stiffening of periarticular connective tissue, however the precise aetiology is unclear. A possible explanation for DIABETES MELLITUS is the non-enzymatic glycation of collagen causing the thickening of ligaments, tendons, joint capsules and skin, thus resulting in LIMITED JOINT MOBILITY. (Duffin et al 1999).

LIMITED JOINT MOBILITY is usually most apparent in the hands of diabetics (Dijs et al 2000). It has been shown to be a useful indicator of risk of early microvascular complications (Rosenbloom et al 1981). It has also been known to affect the cervical and thoracolumbar spine, wrist, elbow, ankle and metacarpophalangeal joints in DIABETES MELLITUS (Duffin et al 1999). Characteristically the patient has tight, thick, waxy skin over the affected joints in both moderate and severely affected groups.

There has been a wide range of methods used to measure LIMITED JOINT MOBILITY using goniometers, custom made measuring instruments, clinical observation or a combination of all of these.

A common clinical way of measuring LIMITED JOINT MOBILITY in the hands is by using the “prayer” sign in which the subject is asked to approximate the palmar surfaces of their hands, actively extending the interphalangeal joint (Duffin et al 1999). The “prayer” sign was first introduced by Rosenbloom et al (1981) to quantify LIMITED JOINT MOBILITY in the hands (Sauseng et al 2002). A positive palmar sign is shown by the presence of a gap between the palmar surfaces, i.e. failure to fully extend the interphalangeal joints. “If such approximation is incomplete, the examiner confirms the limitation by passively extending the patient’s fingers.” (Rosenbloom et al 1981). It is also known as “fanned hand-to-hand” (Simmons et al 1997) and “clapping position” (Starkman et al 1986). In a “normal” subject, extension of the proximal interphalangeal joints is equal to or greater than 180°, and extension of metacarpophalangeal joints is 60° (Rosenbloom et al 1981)

There may be several reasons for LIMITED JOINT MOBILITY in the hands apart frange of movement a peripheral neuropathy. These can include, as cited by Slama et al (1985) and Dijs et al (2000), aging, sex, body mass index (BMI), heavy manual professional work/hobby, Dupuytren’s contracture, osteoarthritis, partial amputations of the hands, excessive scar tissue and significant peripheral vascular disease (Dijs et al 2000; Slama et al 1985). Dijs et al (2000) also mentions the importance of excluding these other conditions when using the “prayer” sign. Conventional neurophysiologic techniques were also carried out to detect any neuropathies. All the measurements should be taken by a single examiner, as was done by Glasoe et al (2002), to help eliminate any variables.

The utility of the “prayer” sign may be questionable. However a weak correlation in diabetics suggesting that “prayer” sign may be a useful measure of more global LIMITED JOINT MOBILITY. was found between the ankle range of motion and the “prayer” sign. Sauseng et al (2002) also suggests using the “prayer” sign as a representable indicator for foot LIMITED JOINT MOBILITY.

In contrast to Rosenbloom et al (1981) the advantage of using only active methods when measuring the “prayer” sign is that the “real daily limitation for the patient” (Sauseng et al 2002) can be determined, whereas by using passive methods “the result depends on the power and sensitivity of the examiner to feel a resistance or to stop when the pain threshold of the patient is reached” (Sauseng et al 2002).

This study set out to investigate if the “prayer” sign is a useful indicator of LIMITED JOINT MOBILITY in a patient group with DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY other than diabetes – HUMAN IMMUNODEFICIENCY VIRUS-infected subjects.

Method

Twenty-four ambulatory subjects with HUMAN IMMUNODEFICIENCY VIRUS-infection were recruited frange of movement the Ian Charleson Day Centre at Royal Free Hospital.

Ethical approval was sought and obtained frange of movement the Royal Free Hospital Ethics Committee and specific precautions were taken to prevent injury frange of movement hyperextension of interphalangeal joints, by explaining exactly what was required as well as a practical demonstration. Instructions were also given to inform the researcher of any pain or discomfort.

All participants signed a consent form, on which it stated that they were not obliged to complete the study. An information sheet was also provided containing details of the experiment, and stating that results were confidential.

This is a simple correlational design with two variables. Vibration Pain Threshold (VPT), a surrogate marker for degree of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY and “prayer” sign score as a measure of LIMITED JOINT MOBILITY of the hands. The hypothesis is one-tailed in that LIMITED JOINT MOBILITY is expected to increase with increasing VPT.

The inclusion criteria for this study were: (1) HUMAN IMMUNODEFICIENCY VIRUS-infection of 2 years or more; (2) aged between 20-60 years old; (3) ability to understand purpose of study and provide informed consent. The exclusion criteria were as follows: (1) any history of trauma to the hands; (2) history of connective tissue and neurological disorders (other than DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY); (3) under 20 years old or over 60 years old; (4) diabetes; (5) dizziness / unsteadiness; (6) arthritis / joint swelling; (7) loss of coordination; (8) amputees.

The VPT data was collected by the supervisor and shared amongst the group of undergraduate students involved in these studies. This also ensured that the “prayer” sign rater was blinded to the VPT readings of each subject.
NPQ was also adiabetes mellitusinistered as part of the overall study but the data collected was not involved in this particular study.

The “prayer” sign score, rated by the undergraduate researcher, was used to measure the participants’ ability to actively hyperextend their interphalangeal joints. This is a valid and reliable way of measuring hyperextension of the interphalangeal joints and is used widely in clinical practice. [Glassoe et al, Sausend et al, Dijs et al, Rosenbloom et al]

A separate pilot study was performed on 6 normal subjects to ensure instructions given were clear and that there was a good flow of procedure.

The Neuropathic Questionnaire was distributed and VPT readings (Neurothesiometer, Horwell Scientific, London) carried out by study supervisor

The neurothesiometer was applied to the dorsum of the first toe proximal to the nail bed and the measurements were taken using the method of limits (Chong, 2004). The voltage was manually increased on the neurothesiometer and the subject indicated when they perceived the vibration sensation. This voltage was recorded. The voltage was then manually decreased on the neurothesiometer and the subject asked to indicate when they perceived the vibration sensation to cease. This voltage was also then recorded. This was repeated three times with a 10 second break between readings.

The student researcher taking the readings for “prayer” sign had no knowledge of the results of VPT readings until all the data collection was complete. This was to ensure no bias. The subject was seated with shoulders in neutral and elbow flexed at 90 degrees and by the side of the body with the hands and forearms supinated resting on the armrests. The hands were placed on a clear sheet of Perspex one at a time, as flat, or as near to flat, as possible with all fingers fanned. This was double-checked by a fellow undergraduate researcher. The operator noted the subject’s ability (or lack of) to flatten hand against the Perspex using the following 3 stages (Rosenbloom et al, Aljahlan et al):
Stage 0: Ability for all interphalangeal joints to contact Perspex.
Stage 1: Inability for one interphalangeal joint to contact Perspex.
Stage 2: Inability for two or more interphalangeal joints to contact Perspex.

Data Analysis
The data collected on “prayer” sign was ordinal data and the VPT was continuous/interval data. Therefore a non-parametric rank correlation – Spearman’s rho was used to analyse the data with a confidence level set at 95% (p<0.05).

Results

All participants were male. One subject was excluded due to a past history of CNS lesions. Another subject was excluded for reporting dizziness on the day of data collection. A further subject was excluded for being too old. Ultimately twenty-one subjects, aged 20-60 years old, were included in this study.

Descriptive Statistics
Table 1

N Minimum Maximum Mean Std. Deviation
VPTMean (volts) 21 3.5 30 9 6.83
minCD4 (cells/ml) 21 69 775 213 160.32
latestCD4 (cells/ml) 21 178 777 466 196.31
Left (“prayer” sign score) 21 0 2 1 0.86
Right (“prayer” sign score) 21 0 2 1 0.93
Both (“prayer” sign score) 21 0 4 1 1.60

Intra-rater reliability
An intraclass reliability collection was performed to ensure reliability and validity of data collection. Five randomly selected non-HUMAN IMMUNODEFICIENCY VIRUS infected subjects were used to take readings of both hands, repeated five times. The intraclass correlation = 1 representing 100% intra-rater reliability.

Table 2
VPTMean Left Right BothHands Age
VPTMean Correlation Coefficient
Sig. (1-tailed)
N
Left Correlation Coefficient 0.360541
Sig. (1-tailed) 0.054184
N 21
Right Correlation Coefficient 0.011486
Sig. (1-tailed) 0.480295
N 21
BothHands Correlation Coefficient 0.204067
Sig. (1-tailed) 0.187465
N 21
Age Correlation Coefficient 0.447626 0.232437 -0.21291 0.022872
Sig. (1-tailed) 0.020937 0.155312 0.177064 0.460804
N 21 21 21 21
* Correlation is significant at the 0.05 level (1-tailed).

All correlations between ““prayer” sign score and VPT failed to reach significance although the correlation between mean VPT and “prayer” sign score for the left hand only almost reached significance with r=0.36 and p=0.054.

Discussion

There is no statistical evidence frange of movement this study to suggest that “prayer” sign as a measurement of LIMITED JOINT MOBILITY in the hands is associated with VPT as a measure of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY. This may imply that LIMITED JOINT MOBILITY of the hands does not exist in HUMAN IMMUNODEFICIENCY VIRUS-infected subjects with DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY in a form similar to that seen in diabetic DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY.

The method of using Perspex to measure “prayer” sign has not been mentioned in any previous published research, but was utilised in this study because it allowed a more visible and clear view of all the interphalangeal joints. Therefore it makes it difficult to accurately compare and contrast the findings of this study with previously published research. Although the intra-rater reliability score was 100%, the method of measuring may be regarded as crude as it only allowed three stages to be defined, despite the fact that each “prayer” sign reading was double-checked by a fellow undergraduate researcher.

As mentioned before, previous studies in DIABETES MELLITUS patients using the “prayer” sign have found increased LIMITED JOINT MOBILITY with increased severity of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY. However as no previous studies have been carried out using subjects with HUMAN IMMUNODEFICIENCY VIRUS-infection, this suggests that there may be differences in the way LIMITED JOINT MOBILITY manifests in DIABETES MELLITUS DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY compared with HUMAN IMMUNODEFICIENCY VIRUS DPSN. Most of the studies did not use VPT, but had subjective information frange of movement the participants about their symptoms or categorised subjects into mild and severe DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY based on composite measures. This prevents close comparison between this and previous studies in DIABETES MELLITUS.

According to Fernando, the “prayer” sign is a useful indicator of LIMITED JOINT MOBILITY only in severe cases of (DIABETES MELLITUS) DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY. In the same study they found a significant difference in LIMITED JOINT MOBILITY “as assessed by the prayer sign, compared to controls”. (Fernando et al 1997).

Other reasons for LIMITED JOINT MOBILITY are manual labour and smoking. Information about these aspects of the lives of the participants was not acquired. Therefore it may be useful to perform further studies in HUMAN IMMUNODEFICIENCY VIRUS patients using a control group. Other information such as date of diagnosis of HUMAN IMMUNODEFICIENCY VIRUS may also provide some better insight into degrees of HUMAN IMMUNODEFICIENCY VIRUS DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY.

LIMITED JOINT MOBILITY is more frequently seen in diabetic patients than in any other population (Fernando et al 1997). So the severity of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY in HUMAN IMMUNODEFICIENCY VIRUS patients may be less than in those with DIABETES MELLITUS.

However, in a study carried out by Starkman et al (1986) found there was no significant difference between LIMITED JOINT MOBILITY and neuropathy in diabetic patients over the age of 40 years. The reason for this was the most severe cases of DIABETES MELLITUS may not have survived to the same age as the milder cases, skewing the cohort towards milder DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY in the older age groups. In addition they did not use the VPT to assess the level of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY in their subjects, but a more subjective questionnaire.

According to Rahman et al the “gold standard” for measuring DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY is using monofilament readings, however this is only in the clinical setting. For research purposes of carrying out quantitative sensory testing, the method used in the current study was the most accurate “gold standard”. Standardisation of measurement equipment and methodology in future studies would allow for better comparison of results.

Multiple regression analysis was not possible as there were not enough participants in sample. This meant the statistical analysis was limited to bivariate regression only. In future studies, the multiple regression analysis may be useful in determining correlation of the following factors: age, severity of DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY, hand dominance, duration of HUMAN IMMUNODEFICIENCY VIRUS infection, treatment for HUMAN IMMUNODEFICIENCY VIRUS. However this was not performed as it is beyond the scope of undergraduate research.

All participants in this study were males therefore any conclusions made frange of movement this study can only be applied to males. Future research may consider recruiting female participants to investigate whether they show similar findings. A larger sample may also give more reliable results, as smaller samples have an increased incidence of being affected by chance.

Although an NPQ was adiabetes mellitusinistered as part of the wider study, the information acquired frange of movement the NPQ was not available to this researcher. This meant that there was no subjective measurement of the participants’ symptomology. It may be useful in further studies, with a larger sample than the current study, to have two groups of participants; one asymptomatic and the other symptomatic. (Kästenbauer et al 2004)

Conclusion

The present study can conclude that there is no evidence to suggest that LIMITED JOINT MOBILITY of the hands, measured using the “prayer” sign, has any correlation with DISTAL SYMMETRICAL PERIPHERAL NEUROPATHY measured using VPT in male patients with HUMAN IMMUNODEFICIENCY VIRUS, aged 20-60 years old.

The findings of this study are of interest to any manual therapies which manipulate joints, e.g. osteopathy, chiropractic, physiotherapy, and may inform future studies of the area of musculoskeletal change associated with HUMAN IMMUNODEFICIENCY VIRUS-infection.

References

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15. Luciano, C.A., Pardo, C.A., McArthur, J.C. (2003). Recent developments in the HUMAN IMMUNODEFICIENCY VIRUS neuropathies. Neurology, 16, pp.403-409.

16. Marchettini, P. (2005). The burning case of neuropathic pain wording. Pain 114, pp.313-314.

17. Rahman, M., Griffin, S.J., Rathmann, W. (2003). How should peripheral neuropathy be assessed in people with diabetes in primary care? A population-based comparison of four measures. Diabetic Medicine, 20, pp.368-374.

18. Rosenbloom, A.L., Silverstein, J.H., Lezotte, D.C., Richardson, K., McCallum, M. (1981). Limited joint mobility in childhood diabetes mellitus indicates increased risk for microvascular disease. The New England Journal Of Medicine, 305 (4), pp.191-194.

19. Sauseng, S., Kästenbauer, T., Irsigler, K. (2002). Limited joint mobility in selected hand and foot joints in patients with Type 1 diabetes mellitus: A methodology comparison. Diabetes Nutrition and Metabolism, 15 (1), pp.1-6.

20. Simmons, R.W., Richardson, C., Deutsch, K. (1997). Limited joint mobility of the ankle in diabetic patients with cutaneous sensory deficit. Diabetes Research and Clinical Practice, 37, pp.137-143.

21. Slama, G., Letanoux, M., Thibult, N., Goldgewicht, C., Eschwege, E., Tchobroutsky, G. (1985). Quantification of Early Subclinical Limited Joint Mobility in Diabetes Mellitus. Diabetes Care, 8 (4), pp.329-332.

22. Starkman, H.S., Gleason, R.E., Rand, L.I., Miller, D.E., Soeldner, J.S. (1986). Limited joint mobility (LIMITED JOINT MOBILITY) of the hand in patients with diabetes mellitus: relation to chronic complications. Annals of the Rheumatic Diseases, 45, pp.130-135.

23. Wulff, E.A., Wang, A.K., Simpson, D.M. (2000). HUMAN IMMUNODEFICIENCY VIRUS-Associated Peripheral Neuropathy. Drugs, 59 (6), pp.1251-1260.

Posted by Mr. Trishul Vadi (Principal Osteopath in West Wickham, Beckenham, Bromley & South East London) on Tuesday, August 3rd, 2010

New Resources Section

Welcome to the new resources section.

Posted by Mr. Trishul Vadi (Principal Osteopath in West Wickham, Beckenham, Bromley & South East London) on Friday, July 16th, 2010

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Osteopath Says

Monday, August 23rd, 2010

Sciatica

Sciatica by definition is pain experienced in the distribution of the sciatic nerve. The sciatic nerve (which is the thickest and longest nerve in the body – as thick as your thumb) runs down the entire back of your leg, dividing off at various points.
There are several reasons why the sciatic nerve can become irritated [...]

Thursday, August 19th, 2010

Obesity & Lower Back Pain

There is extensive documentation on obesity and lower back pain. However the relationship between lower back pain and obesity remains controversial. A Finnish study on young adults looked at the association between the prevalence on lower back pain and weight-related factors.
Obesity causes an excessive mechanical load on the lumbar spine, often resulting in [...]