Saturday, 23 April 2016


Today I will talk about nutrition and dental caries.....

Very few nutritionist talk about this, because there are very few studies being done by researchers and scientist. Which kind of sugar is effecting?? what is the frequency of sugar consumption?? Do fruits and vegetables also effect the teeth and gums??? 

So many queries in mind... lets solve them...  

Oral health is related to diet in many ways, for example, nutritional influences on craniofacial development, oral cancer, dental caries, dental erosion, developmental defects, oral mucosal diseases and oral infectious diseases. Diet affects the integrity of the teeth; quantity, pH, and composition of the saliva. Nutrition affects the teeth during development and malnutrition may exacerbate periodontal and oral infectious diseases. However, the most significant effect of nutrition on teeth is the local action of diet in the mouth on the development of dental caries and enamel erosion. Dental erosion is increasing and is associated with dietary acids, a major source of which is soft drinks. Despite improved trends in levels of dental caries in developed countries, dental caries remains prevalent and is increasing in some developing countries undergoing nutrition transition. There is convincing evidence, collectively from human intervention studies, epidemiological studies, animal studies and experimental studies, for an association between the amount and frequency of free sugars intake and dental caries. Although other fermentable carbohydrates may not be totally blameless, epidemiological studies show that consumption of starchy staple foods and fresh fruit are associated with low levels of dental caries.
Therefore on the basis of the scientific researches, the following recommendations are suggested by me as a nutritionist:
  • High intakes of starchy staple foods, fruits and vegetables are associated with low levels of dental caries.
  • Cooked staple starchy foods such as rice, potatoes and bread are of low cariogenicity in humans.The cariogenicity of uncooked starch is very low. Finely ground and heat-treated starch can induce dental caries but the amount of caries is less than that caused by sugars. 
  • The addition of sugar increases the cariogenicity of cooked starchy foods. Foods containing cooked starch and substantial amounts of sucrose appear to be as cariogenic as similar quantities of sucrose.

  • Animal studies have also been used to investigate the relationship between amount of sugars consumed and the development of dental caries. A research done by Mikx et al. found a significant correlation between the sugar concentration of the diet fed to rats and the incidence of dental caries. According to Hefti and Schmid found that dental caries severity increased with increasing sugars concentrations up a 40% sucrose diet. A number of epidemiological studies provide evidence for an association between amount of sugars consumed and dental caries. 
  • Data from animal studies have indicated the importance of frequency of sugars intake in the development of dental caries. Dental caries experience increases with increasing frequency of intake of sugars even when the absolute intake of sugars eaten by all groups of rats was the same. The frequency of consumption of foods containing free sugars should be limited to a maximum of 4 times per day.
  • Many of the earlier animal studies investigating the relationship between sugars and dental caries focused on sucrose, which was at that time the main dietary sugar that was added to the diet. However, modern diets of industrialised countries contain a mix of sugars and other carbohydrates including sucrose, glucose, lactose, fructose, glucose syrups, high fructose corn syrups and other synthetic oligosaccharides and highly processed starches that are fermentable in the mouth. Oral bacteria metabolise all mono and di-saccharides to produce acid and animal studies have shown no clear evidence that, with the exception of lactose, the cariogenicity of mono and disaccharide differs. However, early plaque pH studies have shown plaque bacteria produce less acid from lactose compared with other sugars.

  • Combining dairy foods with sugary foods, raw foods with cooked and protein-rich foods with acidogenic foods are beneficial.
  • Eating and drinking be followed by cariostatic foods such as xylitol chewing gum is recommended. Sugar-free chewing gum is “toothfriendly” as it helps increase saliva flow and clears food debris from the mouth.
  • Restrict consumption of sweetened beverages during meal and snack time. 
  • Hard cheese increases the flow of saliva. Cheese also contains calcium, phosphate and casein, a milk protein, which protects against demineralisation. Finishing a meal with a piece of cheese helps counteract acids produced from carbohydrate foods eaten at the same meal.
  • Do not nibble food or sip drinks continuously. Allow time between eating occasions for saliva to neutralise acids and repair the teeth.
  • Decrease frequency and contact with acidic foods and drinks
  • Avoid brushing teeth immediately after consuming acidic foods, drinks, citrus fruits and juices. This allows time for remineralisation to occur.
The dental team should thoroughly understand the relationship of diet to caries and conscientiously apply that knowledge to educate the patients in general as well as counsel specific high-risk individuals. Further emphasis should be placed on the acquisition of sound scientific data for counseling caries patients concerning diet and dental caries.
The primary public health measures for reducing caries risk, from a nutrition perspective, are the consumption of a balanced diet and adherence to dietary guidelines and the dietary reference intakes.

  • Mikx FHM, Hoevel JSvd, Plasschaert AJM, Konig KG. Effect of Actinomyces viscosus on the establishment and symbiosis of Streptococcus mutans and Streptococcus sanguis on SPF rats on different sucrose diets. Caries Research 1975; 9: 1–20. 
  • Guggenheim B, Konig KG, Herzog E, Muhlemann HR. The cariogenicity of different dietary carbohydrates tested on rats in relative gnotobiosis with a streptococcus producing extracellular polysaccharide. Helvetica Odontologica Acta 1966; 10: 101–13.
  • Konig KP, Schmid P, Schmid R. An apparatus for frequencycontrolled feeding of small rodents and its use in dental caries experiments. Archives of Oral Biology 1968; 13: 13–26.
  • Holbrook WP, Arnadottir IB, Takazoe I, Birkhed D, Frostell G. Longitudinal study of caries, cariogenic bacteria and diet in children just before and after starting school. European Journal of Oral Sciences 1995; 103: 42–5.
  • Holbrook WP, Kristinsson MJ, Gunnarsdottir S, Briem B. Caries prevalence, Streptococcus mutans and sugar intake among 4-year-old urban children in Iceland. Community Dentistry and Oral Epidemiology 1989; 17: 292–5.
  • Rugg-Gunn AJ, Hackett AF, Appleton DR, Jenkins GN, Eastoe JE. Relationship between dietary habits and caries increment assessed over two years in 405 English adolescent schoolchildren. Archives of Oral Biology 1984; 29: 983–92.  
  • Burt BA, Eklund SA, Morgan KJ, Larkin FE, Guire KE, Brown LO, et al. The effects of sugars intake and frequency of ingestion on dental caries increment in a 3-year longitudinal study. Journal of Dental Research 1988; 67: 1422–9.
  • Ludwig TG, Bibby BG. Acid production from different carbohydrate foods in plaque and saliva. Journal of Dental Research 1957; 36: 56–60.
  • Hussein I, Pollard MA, Curzon MEJ. A comparison of the effects of some extrinsic and intrinsic sugars on dental plaque pH. International Journal of Paediatric Dentistry 1996; 6: 81–6.


Good evening everyone...

Glad to be back again.

After such a long time I m writing an article. It fees so good.

Today I m going to talk about nutritional requirement for pregnant women and Lactating mother. As I am facing the same phase, very exciting, different and always alarming. Taking care of yourself more than anybody else so that the fetus inside me should be safe and happy.

From conception to exclusive breast feeding (first 6 months) the baby completely depends on mother’s nutritional status.  If the mother is overweight, it will decrease the blood circulation to the uterus and restrict the quantity and quality of nutrients transferred to the placenta which further provide nutrients to the fetus. On the other hand, if the mother is underweight or not gaining optimal weight during pregnancy the nutrients that are transferred to the fetus will be of inadequate in context with quality as well as quantity. There is a considerable increase in the nutritional needs of the mother. On an average the pregnant women gains about 10 - 12 kg during pregnancy. A pregnant women need to consume about 350 extra calories per day, which translates to one additional meal. The growth and development of the fetus is determine

d by the food taken by the mother. All the nutrients provided to the baby are derived from her food. In the first seven days, baby nourishes with the nutrients from the just fertilized ovum, then the amniotic fluid and later on throughout the pregnancy the baby receives nutrients via the placenta. Even after birth the baby receives all the nutrients for the first 6 months exclusively from mother’s milk. This is followed by gradual introduction of complementary foods after 6 months along with the mother’s milk. Eating healthily during pregnancy will help the baby to develop and grow normally, and will keep the mother fit as well. A healthy diet during pregnancy should contain the right balance and combination of nutrients. If the mother is consuming a balanced diet comprising of various food groups, she gets the benefit of various nutrients that are necessary and increased during the pregnancy

Adequate intake of a nutritious diet is reflected in optimal weight gain during pregnancy (10 to 12 kg) by the expectant woman. Their diet should be well balanced and include adequate amount of foods from all food groups, i.e. body building foods (Protein), protective foods (Vitamins and Minerals) and energy giving food (Carbohydrates). If mother takes a well balanced diet, she will have a normal course of pregnancy.
Pregnant women should choose foods rich in fiber (fibre 25 g/1000 kcal) like whole grain cereals, pulses and vegetables, to avoid constipation.
Excess intake of beverages containing caffeine like coffee and tea adversely affect foetal growth and, hence, should be avoided. In addition to satisfying these dietary requisites, a pregnant woman should undergo periodic health check-up for weight gain, blood pressure, anaemia and receive tetanus toxoid immunization.
Daily oral iron and folic acid supplementation is recommended as part of the antenatal care to reduce the risk of low birth weight, maternal anaemia and iron deficiency. Iron is needed for haemoglobin synthesis, mental function and body defence. Deficiency of iron leads to anaemia. Plant foods like legumes and dried fruits contain iron. Folic acid, taken throughout the pregnancy, reduces the risk of congenital malformations and increases the birth weight. Green leafy vegetables, legumes, nuts and liver are good sources of folic acid. 500 mg folic acid supplementation is advised preconceptionally and throughout Pregnancy for women with history of congenital anomalies (neural tube defects, Cleft palate). 
Calcium is essential, both during pregnancy and lactation, for proper formation of bonesØ and teeth of the offspring and for secretion of breast-milk rich in calcium and also to prevent osteoporosis in the mother.  Iodine intake ensures proper mental health of the growing foetus and infant.
The pregnant women require enough physical exercise with adequate rest for 2-3 hrs during the day. Pregnant and lactating women should not indiscriminately take any drugs without medical advice as some of them could be harmful to the foetus/baby. Smoking and tobacco chewing and consumption of alcohol must be avoided. Wrong food beliefs and taboos should be discouraged.

A balanced diet suitable for a nursing mother shall contain the same kind of food as those recommended during pregnancy, but slightly increased quantities. Twin factors of physical activity and active production of breast milk make additional demands for energy yielding foods, proteins and other nutrients. A mother's capacity to produce milk of sufficient quantity and quality to support infant growth is resilient and remarkably resistant to nutritional deprivation, however, milk production normally affects maternal body composition and nutritional status, and lactating women have increased nutrient demands.
The women who are breastfeeding her infant requires not only large quantities of body building (Proteins) foods and protective foods (Vitamins and Minerals) but also additional energy yielding foods to facilitates the synthesis and secretion of breast milk.
Intake of fluids should be increased as fluids are essential for adequate milk production. Therefore, consumption of fluids in any form like juices, butter milk, milk and milk based beverages and even plain milk should be encouraged. A mother should preferably take some fluids before breastfeeding her infant
The choice of food is wide during lactation. No food is restricted except highly spiced and strongly flavoured food, as they impart flavour to the milk which may be repulsive to the baby.
They are also given special preparation having ajwain, methi seeds, saunth, til seeds etc, which supply protein, iron, calcium and B-vitamins. These foods are called as galactogogues, i.e foods that help produce more milk.
Small and frequent meals (5-6meals in a day) are recommended. Greenleafy vegetables and fruits of all varieties should be consumed.
Since some of the medicines can be absorbed into the mother’s blood stream and may be secreted in the milk, the use of medicines during lactation should be strictly under medical supervision.

Good nutrition during lactation will not only ensure optimum milk supply for the baby and a healthy and happy infant but also help the mother maintain a good nutritional status.

Saturday, 9 March 2013

Bariatric Surgery and Type 2 Diabetes

 Type 2 diabetes mellitus is a metabolic disorder characterized by insulin resistance and progressive failure of pancreatic beta cells, resulting in hyperglycemia. Obesity, is one of the potent risk factor for type 2 diabetes, contributes to its development by inducing insulin resistance and inflammation, which in turn impair glucose regulation. Bariatric surgery is a weight loss surgery, used as a last resort to treat people who are dangerously obese (carrying an abnormally excessive amount of body fat). This surgery is used to treat people with potentially life-threatening obesity that will not respond to non-surgical treatments, such as lifestyle and dietary changes or modifications. According to guidelines from the National Institutes of Health, the current indications for bariatric surgery include a BMI of 40 kg/m2 or higher, or a BMI between 35 and 40 kg/m2 with at least two obesity-related comorbidities. The guidelines suggest that bariatric surgery be discussed with all severely obese patients (BMI > 35 kg/m2) with type 2 diabetes who have not been able to lose weight with other weight-control approaches.
In bariatric surgery, weight loss is usually achieved by reducing the size of the stomach with an implanted medical device (gastric banding) or through removal of a portion of the stomach (sleeve gastrectomy or biliopancreatic diversion with duodenal switch) or by resecting and re-routing the small intestines to a small stomach pouch (gastric bypass surgery). But not all bariatric procedures have the same effect on weight and diabetes.
The recent researches revealed that after bariatric surgery, patients lose more weight than with traditional weight-loss methods—up to 25% of their total body weight. Furthermore, of those with type 2 diabetes, 87% achieve at least better glucose control and need fewer antidiabetic medications, and an average of 78% achieve normal glycemic control without taking any antidiabetic medications at all.

There are three major mechanisms or theory that explains how bariatric surgery reverses diabetes. 1st theory indicates weight loss increases insulin sensitivity. The negative energy balance and weight loss after bariatric surgery reduce insulin resistance. Consequently, the beta cells can rest because they don’t need to produce as much insulin. Usually observed after both gastric restrictive procedures and gastric bypass procedures. 2nd theory reflects that bariatric surgery lessens insulin resistance by reducing “lipotoxicity,” a condition related to dysregulated fatty acid flux, lipid metabolites in tissues, and direct and indirect effects of hormones secreted by adipocytes. The strongest evidence for this theory comes from Bikman et al, who found that insulin sensitivity increased after Roux-en-Y surgery more than expected from weight loss alone. One year after surgery, even though they remained anthropometrically obese (BMI > 30 kg/m2), the patients had insulin sensitivity levels similar to those in a control group of lean people (BMI < 25 kg/m2).
The third theory is likely the most relevant and relates to various hormones secreted by the gut in response to food. Surgical exclusion of the duodenum in the Roux-en-Y procedure and of the duodenum and jejunum in biliopancreatic diversion result in altered relative distribution of CHO and fat absorption. The “hindgut hypothesis” raised by Cummings et al, suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances, which account for the reversal of hyperglycemia and obesity. In contrast, the “foregut hypothesis” raised by Rubino et al, suggests that nutrient interactions in the duodenum are diabetogenic and, hence, bypassing the duodenum would reverse this defect.
Strong evidence now exists that bariatric surgery increases life expectancy and that this is largely attributable to reduction in CVD risk factors such as diabetes and cancer. Recent studies have found that the long-term death rate is 32% to 73% lower for patients undergoing bariatric surgery than in matched controls who do not undergo surgery. A decrease in the death rate related to diabetes has played an important role in these results.
  1. Adams TD, Gress RE, Smith SC, et al. Long-term mortality after gastric bypass surgery. N Engl J Med 2007; 357:753–761.
  2. Bikman BT, Zheng D, Pories WJ, et al. Mechanism for improved insulin sensitivity after gastric bypass surgery. J Clin Endocrinol Metab 2008;93:4656–4663.
  3. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA 2004; 292:1724–1737.
  4. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med 2009;122:248–256.
  5. Consensus Development Conference Panel. NIH conference. Gastrointestinal surgery for severe obesity. Ann Intern Med 1991; 115:956–961.
  6. Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypass for obesity: mechanisms of weight loss and diabetes resolution. J Clin Endocrinol Metab 2004; 89:2608–2615.
  7. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am 2004; 88:787–835.
  8. Kashyap SR, Defronzo RA. The insulin resistance syndrome: physiological considerations. Diab Vasc Dis Res 2007; 4:13–19.
  9. Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA 2003; 289:76–79.
  10. Rubino F, Forgione A, Cummings DE, et al.The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg 2006;244:741–749.
  11. Sjöström L, Narbro K, Sjöström CD, et al., Swedish Obese Subjects Study. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med 2007; 357:741–752.
  12. Unger RH. Minireview: weapons of lean body mass destruction: the role of ectopic lipids in the metabolic syndrome. Endocrinology 2003;144:5159–5165.

Tuesday, 14 August 2012



What kind of name is this – MONK FRUIT????

When I heard this name… I was surprised too…

One of my brilliant student, Ishu Gupta asked me about this fruit. Seriously, I had no idea what this fruit was all about??? Why it’s called as monk fruit?? Where it produce?? What medicinal properties this fruit has??? Etc.. Etc… so many questions???

So, finally I did a lot of research on this monk fruit with the help of Google and pub med, and trust me, I was astonished by its properties...

Here I am…

MONK FRUIT (Siraitia grosvenorii)

Monk Fruit is also known as Luo Han Guo (luohanguo) refers to the fruit of Siraitia grosvenori, formerly called Momordica grosvenori, a member of the Curcubitaceae. Monk fruit has traditionally been grown on steep forested mountains in small family orchards. According to legend, monk fruit is named after the Buddhist monks who first cultivated it nearly 800 years ago. Ever since then it has been treasured for its health-giving powers and its unique low-calorie sweetness. Monk fruit (Luohanguo) is primarily grown in southern China, mainly in Guangxi Province, with most of the product from the mountains of Guilin. The steep mountains provide shade and they are frequently surrounded by mists that further protect against excessive sun, yet the temperature in this southern province is warm. The wild plant is rare, thus luohanguo has been cultivated in the region for many years. With the time, the plant also travelled to a few more countries in the South –East Asia but most parts of the world are still unaware of it. In fact the world came to know about this fruit barely a hundred years ago.
The outer surface of the dried Monk fruit is round and smooth, dusty yellow-brown or dusty green-brown. It is covered with fine, soft hair. The fruit is covered by a hard but thin shell. Inside is a partly dry, flexible substance containing the juice, as well as a large number of seeds. The skin, juicy part, and seeds all have a good sweet flavor. Its nature is cool, and it has no poison.

Monk fruit have some really good properties. Some of them are:-

Natural sweetener -The monk fruit act as a natural sweetener. Monk fruit extract is a high intensity, zero-calorie sweetener, and can be used in blends with sucrose, fructose and erythitol. The sweetness of this fruit is due to the presence of achemical mogrosidein its pulp. The pulp of this fruit contains around 1% mogroside making it the sweetest fruit on earth. Both the fresh and dried fruits are extracted to yield a powder that is 80% or more mogrosides. The mixed mogrosides are estimated to be about 300 times as sweet as sugar by weight, so that the 80% extracts are nearly 250 times sweeter than sugar; pure mogrosides 4 and 5 may be 400 times as sweet as sugar by weight.

Good for diabetic patients - Diabetes is a common endocrine-metabolic disease with rising incidence in recent years. It is the third most life threatening disease whose mortality is right after cancer and cardiovascular disease. Research and development of drugs against diabetes and its complications have been getting more and more attentions.
Guo-Ping Lin etal (2007) conducted a study on Effect of Siraitia grosvenorii Polysaccharide on Glucose and Lipid of Diabetic Rabbits Induced by Feeding High Fat/High Sucrose Chow. The Siraitia grosvenorii polysaccharide (SGP) from the Siraitia grosvenorii (Swingle) was isolated and purified. The therapeutic effects of SGP on diabetic rabbits induced by feeding high fat/high sucrose chow were studied. The study concluded that SGP not only ameliorates the lipid disorder, but also lowers plasma glucose levels. So SGP have obvious glucose-lowering effect on hyperglycaemic rabbits induced by feeding high fat/high sucrose chow, its mechanism may be related to amelioration of lipid metabolism and restoring the blood lipid levels of hyperglycaemic rabbits.

 TheMonk fruit helps relieve sunstroke, moistens the lungs, eliminates phlegm, stops cough, and promotes bowel movements.

These are some of the benefits of this fruit…

But I feel we need to do some more researches on medical properties of monk fruits. As in my knowledge, there is only 1 research study available in database that stated monk fruit have good effects on diabetes. If we conduct researches, keeping in mind, its sweetening properties, then I think we don’t need artificial sweeteners for diabetic patients, monk fruit will work perfectly – that my hypothesis… what u think?????

Image courtesy:,,,

T. Tsurtematsu and A. Shigenobu, “Study on the constituents from fructs of momordicae grosvenori,” Pharmaceutical Journal, vol. 103, pp. 1151–1173, 1983.

R. Kasai, R.-L. Nie, K. Nashi, et al., “Sweet cucurbitaneglucosides from fruits of Siraitia siamensis,” Agricultural and Biological Chemistry, vol. 53, no. 12, pp. 3347–3349, 1989.

L.-Q. Zhang, X.-Y. Qi, W.-J. Chen, and Y.-F. Song, “Effect of Mogroside extracts on blood glucose, blood lipid and antioxidation of hyperglycemic mice induced by Alloxan,” Chinese Pharmacological Bulletin, vol. 22, no. 2, pp. 237–240, 2006.   

Thursday, 31 May 2012



Today, I am here to share something latest and new advancement in our medical field. I am really astonished to discover that recently, scientists of Newcastle University have created a video game which helps in recovery of stroke patients.

A stroke happens when blood flow to a part of the brain stops. A stroke is sometimes called a "brain attack." If blood flow is stopped for longer than a few seconds, the brain cannot get blood and oxygen. Brain cells can die, causing permanent damage. There are two major types of stroke: ischemic stroke and hemorrhagic stroke.
Ischemic stroke occurs when a blood vessel that supplies blood to the brain is blocked by a blood clot.
A hemorrhagic stroke occurs when a blood vessel in part of the brain becomes weak and bursts open, causing blood to leak into the brain.
Stroke-related impairment often restricts patients from properly participating in the activities of daily living, and impedes social interactions. Motor deficits of the hands and upper extremities are important determinants, and strongly represent one’s ability to regain independence in daily and social living. Previous reports describe that approximately 60–70% of stroke patients exhibit mild to severe hand dysfunction; and up to 20% of stroke survivors were dependent in their basic daily living activities.
There are number of researches conducted to analyze and find out the effective treatment for stroke patients to recover as soon as possible. Some of them are-

A research conducted by Hsiu-Yun Hsu etal (2012) investigated the hand movement dynamics  and to develop effective therapeutic interventions for stroke patients published in the Journal of NeuroEngineering and Rehabilitation. They used a custom-designed computerized evaluation and reeducation biofeedback (CERB) prototype to analyze hand grasp performances, and monitor the training effects on hand coordination for stroke patients with sensory disturbance and without motor deficiency. The research concluded that the CERB prototype can provide momentary and interactive information for quantitative assessing and re-educating force modulation appropriately for stroke patients with sensory deficits. Furthermore, the patients could transfer the learned strategy to improve hand function.

Another research conducted by Alma S Merians etal (2011) worked on Robotically facilitated virtual rehabilitation of arm transport integrated with finger movement in persons with hemiparesis published in the Journal of NeuroEngineering and Rehabilitation.  They worked on twelve subjects post-stroke were trained for eight days on four upper extremity gaming simulations using adaptive robots during 2-3 hour sessions. Concluded that Complex gaming simulations interfaced with adaptive robots requiring integrated control of shoulder, elbow, forearm, wrist and finger movements appear to have a substantial effect on improving hemiparetic hand function.

But recently the “circus challenge” computer game is created by the scientists of Newcastle University. These are the first action video games designed specifically to be played at home and to provide an expert therapy programme. Using wireless controllers, players try their hand at such activities as lion taming, juggling, plate spinning, high diving and flying the trapeze and by working their way through increasingly difficult levels of Circus Challenge the movements required are designed to gradually build up the strength and skills of the patient. The games gradually increase in difficulty and complexity to ensure that the stroke patient is always being challenged - but most importantly the games are designed to be fun.

Janet Eyre, Professor of Paediatric Neuroscience at Newcastle University, who also works within the Newcastle NHS Hospitals Foundation Trust, set up Limbs Alive Ltd to produce the first suite of games in association with a professional game studio. He stated that “With our video game, people get engrossed in the competition and action of the circus characters and forget that the purpose of the game is therapy.” Further he added that “Patients who have played the games find them easy to use, challenging and fun! They can be easily set up and played at home since they are designed by a professional games studio to be played on a laptop or PC. Patients forget they’re doing therapy and just enjoy the challenge of playing.”


Hunter SM, Crome P: Hand function and stroke. Rev Clin Gerontol 2002, 12:68–81.

Nakayama H, Jorgensen HS, Raaschou HO, Olsen TS: Recovery of upper extremity function in stroke patients: the Copenhagen Stroke Study. Arch Phys Med Rehabil 1994,

Wade DT, Langton-Hewer R, Wood VA, Skilbeck CE, Ismail HM: The hemiplegic arm after stroke: measurement and recovery. J Neurol Neurosurg Psychiatry 1983, 46:521–

Duncan PW, Badke MB (Eds): Stroke Rehabilitation: The Recovery of Motor ControlChicago: III.: Year Book Medical Publishers; 1988.

Rosamond W, Flegal K, Furie K, Go A, Greenlund K, Haase N, Hailpern SM, Ho M, Howard V, Kissela B, et al: Heart disease and stroke statistics2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008, 117:e25–e146.

Trombly CA: Deficits of reaching in subjects with left hemiparesis: a pilot study. Am J Occup Ther 1992, 46:887–897.

Johansson BB: Current trends in stroke rehabilitation. A review with focus on brain plasticity. Acta Neurol Scand 2011, 123:147–159.

Images courtesy:,