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Biopsies are also useful in confirming cases of certain lesions resulting from infections such as syphilis symptoms genital warts cheap lithium 300 mg with visa, tuberculosis medicine you can overdose on discount 300mg lithium overnight delivery, deep fungal infections medicine 0027 v lithium 150 mg low price, and some lesions of mucocutaneous vesiculobullous type medications without doctors prescription discount lithium 300 mg otc. Histopathological diagnosis also helps to reassure the patient and helps instill a greater degree of confidence in the treatment modalities treatment keratosis pilaris generic lithium 150 mg on-line. Sometimes medications equivalent to asmanex inhaler order lithium 150 mg overnight delivery, a lesion may heal with a therapeutic trial, and a therapeutic diagnosis may be made. But if the disease recurs, then the clinician is again in a dilemma about the diagnosis. People who are given information about the planned investigations and treatment are usually less anxious. When patients are told that they require a biopsy they are usually concerned about both the procedure and the results. Any invasive/surgical procedure is linked to stressors such as pain, cost of treatment, fear of needles, failure of the surgeon and fear of infectious diseases[13]. So, the decision to perform a biopsy should be based on sound evidence from examination and other investigations in order to avoid putting the patient through unnecessary stress associated with the invasive procedure [14]. Pitfalls and complications associated with a biopsy: In spite of being the gold standard, histopathology is subjective and results may not accurately represent severity of lesions. Since sample is taken only from a localized area, the results may overdiagnose or underdiagnose the lesion. Histological assessment alone cannot predict the transformation of an oral lesion into a malignancy. Similar ulceration, necrosis and epithelial sloughing may be present in vesiculobullous disorders. Palatal and gingival biopsies heal by secondary intention and may cause delayed healing, exposure of denuded bone for several weeks or may result in unesthetic gingival recession and root exposure. Tongue lesions cause difficulties in stabilization, suturing with increased risk of the wound reopening. Incorrect handling and fixation can induce artefacts and render the tissue non-diagnostic. Some patients may also report paresthesia following biopsy which may last several days to months. The epithelial changes seen in mucosa with a leukoplakic lesion allows Candida to infiltrate and invade the mucosal surface. An initial exfoliative cytology done to detect the presence of Candida can help to prescribe a topical antifungal agent for an initial period of 2 weeks following which a biopsy can be done. Oral Lichenoid reactions may be induced by either a systemic medication or topical antigen exposure. Withdrawal of the drug or removal of the triggering agent usually resolves the condition. Common anatomical sites include the lateral border of tongue and the buccal mucosa which may be in direct contact with the surface of the restorations. They may also be caused by use of systemic medication and substances like cinnamon. It is therefore essential for the clinician to be familiarized with the individual variations in the clinical presentation of a lichenoid reaction in order to avoid an unnecessary invasive biopsy. The most common cause of a solitary ulcer is chronic trauma resulting from sharp cusp margins, broken teeth or ill-fitting dentures. Other less common causes include a traumatic ulcerative Indian Journal of Public Health Research & Development, January 2020, Vol. Usually ulcers of traumatic origin are soft on palpation and may have rolled margins and keratinization in the surrounding mucosa. The lesion may sometimes be firm with indurated margins, thereby mimicking a malignancy. A period of 2-3 weeks can be given for the chance to heal after elimination of the local factor. Necrotizing sialometaplasia is a benign self-limiting, inflammatory lesion of the salivary gland tissue where there is squamous metaplasia of the ducts and acini after ischaemic necrosis of the salivary gland lobules, most frequently occurring on the hard palate. It may clinically mimic a malignant ulcer but a history of local trauma like administration of local anaesthetic, ill-fitting dentures, intubation or surgical procedures will be present. Socket Granuloma / Overhanging Clot occur as post-operative complications 1-3 days following a tooth extraction, usually as a consequence of not following post-operative instructions. They may give the appearance of a proliferative lesion arising from the socket, prompting the clinician to perform a biopsy. An overhanging clot may need to be removed followed by placement of sutures along with local haemostatic measures or it may resolve on its own. The dentist should therefore be familiar with the incidence of post-operative complications and their management. They are poorly responsive to steroids and only respond to discontinuation or reduction in the dose of the drug. Therefore, careful probing about the history is important to diagnose these cases. When the history and clinical presentation is "classic", biopsy can be deferred until a therapeutic trial is given in the initial visits. If these situations are encountered clinically, the dentist can render invaluable service to the patients with diagnosis and prompt treatment. Ethical Clearance: Not required Conflicts of Interest: None Source of Funding: Self References 1. Immediate biopsy versus a therapeutic trial in the diagnosis and treatment of vesiculobullous/vesiculoerosive oral lesions. Malignant potential of oral lichen planus: observations in 722 patients from India. Biopsy of the oral mucosa and use of histopathology services: Biopsy and histopathology services. Oral lichenoid lesions: Clinico-pathological mimicry and its diagnostic implications. A case of necrotizing sialometaplasia clinically mimicking a malignant tumor of the palate. Poor oral health can complicate the underlying systemic condition and cause deterioration of general health. Dental treatment of people who are medically compromised, disabled or older poses challenges as they might require multiple interventions and are less likely to receive adequate care compared to their apparently normal counterparts. The solution is to have a speciality designed specifically to treat these patients by training professionals in treatment of patients with special needs. Oral Medicine is the speciality concerned with dental and "medical" related disorders of the oro-facial region, including oral manifestations of systemic disease and management of medically complex patients. One of the competencies of an Oral Medicine graduate is the ability to effectively manage patients with medically complex conditions and special needs. Oral Medicine specialists may be considered the best choice for integration with the field of Special Care Dentistry as they have knowledge on medical diseases and their effect on oral health. This paper highlights the need for Special Care Dentistry in the Oral Medicine Curriculum and why Oral physicians are best suited for provision of dental care in this population. Keywords: Special Care Dentistry, Oral Medicine, Oral Physician, Special Needs, Medically Compromised. Disability is diverse and includes any condition that restricts everyday activities, an impairment that may be cognitive, intellectual, physical, mental, and sensory or a combination of the above. Disability rates continue to rise around the world due to the increase in life expectancy, the ageing population and increased likelihood of acquiring chronic diseases. Oral health in these people as they are often unemployed, earn less, have difficulties in communication, transport and usually depend on caretakers for help and support. So, they may require additional and specific care when compared to the general population. As professionals, we have the responsibility to ensure that the oral health care needs of these people are met and treatment is best when provided by a professional with adequate training in handling patients with special health care needs. It also includes people with complex health conditions, people under long term hospitalization and critical care and people in residential care units. The United States has founded the American Board of Special Care Dentistry and training programmes have been offered in numerous universities. They also have founded the Special Care Dentistry Association, which is an international organization of oral health professionals who are dedicated to providing and promoting oral health for patients with special oral health care needs. Universities in Australia and New Zealand provide postgraduate courses in Special Needs Dentistry and Hospital Dentistry. According to the 2001 census, 21 million people in India have some form of disability constituting 2% of the world population and 75% of these people are concentrated in the rural areas. A formal organization for treating oral problems of these patients has still not been organized. The physical, mental and medical disabilities make it difficult for the patients to visit a dental office and they are also limited in their ability to afford therapeutic and preventive treatment. A more important factor is dental students not being exposed to caring for the disabled during undergraduate or postgraduate training. Most of the work with disabled persons is estimated to be treatable by general practitioners but the issue here is their little experience in handling these patients. Ensuring that the dental team knows how to manage such situations can be life-saving. Having positive attitudes, positive experiences and positive social contact has been shown to improve interest in serving these populations. Clinical contact with older and disabled people, positive clinical experiences are essential for students to overcome anxieties and develop Indian Journal of Public Health Research & Development, January 2020, Vol. Practitioners may abstain from treating these patients if they felt that these issues have not been resolved. Development of a discipline may aid in the development of specialist services for patients with complex dental needs. It is estimated that 90% of people requiring Special Care Dentistry should be able to access treatment in a local, primary care setting. Provision of such primary care is only possible through the education and training of dentists. The literature suggests that it is vital for the dental team to develop the necessary skills and gain experience treating people with special needs in order to ensure access to the provision of oral health care. Oral medicine and the potential role of oral physicians in special care dentistry Dr. Lester Burket, a pioneer in the field of Oral Medicine, considered by many to be the father of this discipline, was one of the first educators to promote the concept of integration of medicine into dental education and clinical practice. Clinicians manage oral mucosal disease, salivary gland disorders, facial pain syndromes and also provide dental care for patients with complicating medical disease. Unfortunately in our country lack of access to primary medical / dental care prevents patients from seeking treatment until a negative event or complication has occurred. So the best way is to create awareness among patient and for dental professionals to have a clear understanding of the chronic conditions that affect the oral and systemic health of the patient. Since Oral Medicine is the intersection of medicine and dentistry and a window to the general health of the patient, we may be the best suited among all specialities to provide dental care for medically compromised patients. The American Academy of Oral Medicine has described clearly defined minimum competencies that are required of all individuals to successfully complete an Oral Medicine Training program. The scope of Oral Medicine was divided into three domains that represent required clinical expertise. Diagnosis and Non surgical management of oral mucosal and salivary gland disorders. Diagnosis and Non surgical Management of temporomandibular disorders, orofacial pain and orofacial neurosensory disorders. They must assess wound healing, risk of infection, bleeding risk, medication/drug interactions and behavioural issues. This comprehensive evaluation should be accompanied by diagnostic tests and expert medical consultations when indicated. The clinician will then apply this knowledge to implement modifications that are necessary in delivery of dental treatment. Several recent reviews have discussed the nature and extent of training Oral Medicine graduates and the need to further enhance their curricula. A review of the oral health of individuais with disabilities in Puerto Rico and among U. As the only speciality at the crossroads of Medicine and Dentistry, we are already positioned to diagnose and treat oral/systemic conditions. Having a unified speciality could be a referral point for the medical fraternity and improve communication. In addition, training in Special Care Dentistry could help bring out robust professionals who are competent in handling patients with disability and provide graduates with better career opportunities. Ethical Clearance: Not required Conflicts of Interest: None Source of Funding: Self 9. The value of education in special care dentistry as a means of reducing inequalities in oral health: Value of education in special care dentistry. Competencies for the new postdoctoral Oral Medicine graduate in the United States. An international survey in postgraduate training in Oral Medicine: Postgraduate training in Oral Medicine. To access lifestyle changes among the girl child, different lifestyle diseases and their impact on health will be emphasized. Lifestyle is an individually constructed behaviour that determines the health and well-being of an individual. Health of the girl child is determined by a wide range of factors like family background, their socialization process, social class, peer group influence and their like. Girl child in urban India is more vulnerable to lifestyle diseases owing to lack of physical activities and improper food habits resulting due to transformation in consumption pattern.
Dupuytren contracture Dupuytren contracture is a fibroproliferative disorder of the palmar fascia leading to formation of palmar nodules denivit intensive treatment generic 300 mg lithium with visa, development of a palmar aponeurosis cord with tethering of the overlying skin and eventually flexion contractures medicine lodge kansas order lithium 150mg with visa, particularly affecting the ring and little fingers [53] symptoms 7 weeks pregnancy 150 mg lithium otc. Stenosing tenosynovitis (trigger finger) Trigger finger is "a condition in which the flexor tendon is prohibited from gliding through the tendon sheath because of thickening of the synovial sheath over the tendon" [65] symptoms queasy stomach purchase 300 mg lithium with amex. This disorder most frequently affects the ring finger treatment 3 phases malnourished children cheap lithium 300 mg overnight delivery, but can also affect the other fingers and the thumb treatment urticaria quality lithium 150 mg. The patient may report a clicking sensation when moving the finger, discomfort over the palm or overt triggering when the finger is locked in flexion [66]. The syndrome occurs as a result of a discrepancy between the flexor tendon and its sheath in the A1 pulley at the level of the metacarpal head [66]. The pulley becomes thickened with increased extracellular matrix and fibrocartilage metaplasia [67]. Corticosteroid injection into the tendon sheath is an effective therapy for the majority of patients, particularly in the presence of nodular disease. If conservative therapy fails, release using a percutaneous needle approach or open surgery is indicated [69]. Patients with diabetes are at higher risk of trigger finger, with a lifetime risk of 10% compared to 2. Patient age, diabetes duration and presence of microvascular complications are associated with increased risk of trigger finger in diabetes [62,70]. Compression within the carpal tunnel leads to disordered microvascular supply of the nerve, causing demyelination and axonal degeneration. The typical presentation is hand parasthesia, particularly affecting the thumb, index finger and middle finger. Wrist and hand pain may also occur, and patients frequently report hand clumsiness. Clinical examination may be normal, but in the presence of severe and prolonged disease there may be features of median nerve denervation, including thenar wasting, weakness of thumb abduction and sensory loss over the median nerve distribution. Provocative tests including Phalen and Tinel tests may be positive, and if present have relatively high specificity for carpal tunnel syndrome. The Tinel test is positive if paresthesia is reported after tapping the volar wrist over the carpal tunnel. The diagnosis is confirmed by nerve conduction testing, with the typical findings of prolonged latencies and delayed conduction velocities affecting the median nerve across the wrist [76]. Treatment consists of maintaining the wrist in a neutral position using a removable wrist splint. Splinting is particularly useful for nocturnal symptoms, and may be sufficient to treat mild disease [77]. Although oral corticosteroids have short-term efficacy, side effects are usually unacceptable [78]. Surgical release under local anesthesia is a well-tolerated and effective therapy, which should be considered in patients who have failed conservative therapy or have severe symptoms and signs of nerve compression [80]. Carpal tunnel syndrome may be caused by a number of factors including non-specific flexor tenosynovitis affecting the wrist, rheumatoid arthritis and other inflammatory synovial arthropathies, obesity, pregnancy and disordered wrist anatomy [74]. Diabetes is one of the most common metabolic disorders associated with carpal tunnel syndrome, being present in 16% of affected patients [82]. A recent survey using clinical and neurophysiologic assessment reported a prevalence of carpal tunnel syndrome of 2% in a reference population without diabetes, 14% in patients with diabetes but no diabetic polyneuropathy, and 30% in patients with diabetic polyneuropathy [85]. Carpal tunnel syndrome is associated with duration of diabetes, and is more frequently present in patients with microvascular complications such as retinopathy, nephropathy and polyneuropathy [62,86]. Carpal tunnel syndrome is also more common in patients with limited joint mobility, and it has been postulated that this disorder occurs at higher frequency in diabetes because of accelerated thickening and fibrosis of the flexor tendon sheaths within the carpal tunnel [18]. Glycosylation of collagen may also reduce compliance of connective tissue within the carpal tunnel [84]. In addition, the presence of existing microvascular disease may further increase the risk of endoneural ischemia as the median nerve travels through the carpal tunnel. Carpal tunnel syndrome may be more difficult to assess in patients with coexistent diabetic neuropathy, because of atypical presentation and neurophysiologic assessment [85,87]. Treatment options for patients with diabetes and carpal tunnel syndrome are similar to those for patients without diabetes, and responses to surgery are usually good [88,89]. Disorders of joints Charcot joint Charcot joint is a destructive arthropathy, most commonly affecting patients with diabetes in the presence of severe peripheral neuropathy. The developmental stage presents as acute inflammation with swelling, warmth and erythema of the foot. Gradually worsening deformity occurs, with bone resorption, fracture and dislocation, leading to instability of the foot and the classic rocker-bottom dislocation of the midfoot. As deformity develops, radiographs show severe osteolysis, bone fragmentation and disordered architecture (Stage 1). In the coalescence phase (Stage 2), hyperemia resolves, swelling reduces and skin temperature normalizes. The reconstructive stage (Stage 3) is characterized by remodeling of bone, ankylosis and proliferation of bone, and formation of a stable foot. During both the acute and the reparative phases of disease, bony deformity may lead to abnormal load bearing, with ulceration of overlying skin and secondary osteomyelitis. Treatment during the acute phase consists of immobilization which reduces inflammation, prevents abnormal load-bearing and stabilizes the foot in a position of least deformity. The standard immobilization method during the acute phase is a nonweightbearing total contact cast. This treatment requires close monitoring and regular adjustment, and should be maintained until swelling and temperature normalize, and radiographs show no further bony destruction [105]. Some recent uncontrolled reports have indicated that use of a weightbearing total contract cast may be an acceptable alternative to the non-weightbearing option, but controlled trials are not yet available [106,107]. The recognition that the acute phase of Charcot joint is associated with excessive osteoclast activity has led to the testing of agents targeting bone turnover for treatment of this condition. Two randomized controlled trials of bisphosphonates have been reported, and both show efficacy. A single intravenous infusion of 90 mg pamidronate in a study of 39 patients with acute Charcot joint led to significant improvements in symptoms and bone turnover markers [108]. In a study of 20 patients with acute Charcot joint, weekly oral administration of 70 mg alendronate for 6 months was associated with significant improvements in pain scores, bone turnover markers and foot bone density [109]. A randomized trial of intranasal calcitonin demonstrated efficacy with respect to bone turnover markers, but no differences in clinical variables were reported [110]. In general, surgical management is currently recommended for patients in the reparative (rather than the acute) phase of disease, and particularly for patients with deformities associated with chronic foot ulcers and joint instability. Various surgical approaches to arthrodesis may be used, including open reduction with both internal and external fixation, depending on the presence of local infection and other anatomic variables [112]. Other surgery includes exostotomy, osteotomy, intramedullary rodding and amputation. Infection, non-union and triggering of an acute Charcot reaction are important postoperative complications, and careful postoperative management is essential. A recent analysis of 115 patients reported that non-operative management was associated with a 2. Note the osteolysis, bone fragments, subluxation and fracture affecting the tarsometatarsal joints of the foot. Minor trauma frequently precipitates onset of disease, and may lead to subclinical bone injury that triggers an aberrant inflammatory response [96]. It is likely that disordered weight-bearing in joints affected by peripheral neuropathy leads to repetitive injury and instability (the neurotraumatic hypothesis). Additionally, autonomic dysfunction causing vasodilatation, arteriovenous shunting and hyperemic bone resorption has been implicated (the neurovascular hypothesis). Development of osteopenia and osteolysis increases risk of fractures in the presence of abnormal load-bearing with a cycle of joint instability and fracture development, causing further abnormal load-bearing [97]. Recent work has focused on the role of local inflammation in disease pathogenesis. Large numbers of osteoclasts are present within affected bone, and patients with Charcot joint have increased ability to form peripheral blood derived osteoclasts in vitro compared with diabetic and non-diabetic controls [101,102]. Markers of bone resorption are increased in patients with acute Charcot joint [103]. Interestingly, acute phase markers are not significantly elevated, indicating an apparent dissociation between local and systemic inflammatory disease [104]. In early disease, gout presents as recurrent episodes of selflimiting acute inflammatory attacks ("flares") of arthritis. In the presence of prolonged hyperuricemia, some patients develop recurrent polyarticular attacks, chronic tophaceous disease and erosive arthritis (Figure 48. Promotion of renal tubular reabsorption of uric acid by insulin is thought to mediate this relationship [123]. Key risk factors for gout in this population were male sex, renal impairment and diuretic use. Fewer than half of the patients with gout and diabetes in this study were pre- scribed urate-lowering therapy, and only 8% had a serum urate of <0. Interestingly, severe hyperglycemia may reduce urate concentrations, as glycosuria has a uricosuric effect. Thus, as glycemic control improves in patients initiating treatment for diabetes, there is a potential risk of worsening gout attacks [126]. Long-term urate-lowering therapy is indicated for patients with gout who have recurrent flares, gouty arthropathy, tophi or radiographic damage. Allopurinol is the mainstay of urate-lowering therapy, but may be ineffective at recommended doses. If the serum urate target is not achieved with allopurinol alone, further options include dose escalation of allopurinol, addition of a uricosuric agent such as probenecid or benzbromarone, or consideration of the new xanthine oxidase inhibitor febuxostat [128]. Initiation of urate-lowering therapy is frequently associated with exacerbation of gout flares; this side effect can be avoided by commencement of urate-lowering therapy once the acute flare has resolved, gradual introduction of the urate-lowering drug, and co-prescription of low dose colchicine. In addition to the dietary restrictions required for glycemic control, these patients also need to avoid alcohol and purine-rich foods. Diuretic therapy may exacerbate hyperuricemia and should be avoided in patients with gout unless absolutely required. Drugs such as losartan and fenofibrate have weak urate-lowering effects and may be of particular benefit in patients with diabetes and gout if antihypertensive or lipid-lowering therapy is required [129,130]. Ossification of the anterior longitudinal ligament of the spine occurs, most commonly in the thoracic spine (Figure 48. The prevalence has been reported to be as high as 15% in women and 25% in men over the age of 50 [145]. Rare complications such as dysphagia, vocal cord paralysis, compression of the inferior vena cava and neurologic compression syndromes have been described in patients with florid hyperostosis [148]. Spinal fracture may occur after relatively minor injury and cause significant neurologic compromise [149]. The diagnosis is made radiographically, according to the Resnick criteria, which in brief are: 1 Presence of flowing calcification and ossification along the anterolateral aspects of at least four contiguous vertebral bodies; 2 Relative preservation of intervertebral disc height and the absence of extensive degenerative disc disease; 3 Absence of features of spondyloarthropathy [150]. A small uncontrolled study of patients reported that a physiotherapy program focusing on spinal mobility, stretching and strengthening had some benefits in improving lumbar spinal mobility after 24 weeks, with no significant benefits in pain or functional outcomes [151]. Surgery is rarely required, but may be indicated for compressive syndromes caused by florid hyperostosis. It is likely that obesity has direct biomechanical effects, because of increased load at the entheses. Osteoporosis and fractures Background Fragility fractures are a major cause of morbidity and public health expenditure. The most devastating fracture, that of the proximal femur, is associated with a 20% risk of dying within 6 months of the event, and a substantial risk of loss of independence [162]. Individual fractures are associated with considerable periods of disability and loss of productivity [163]. The number of fractures occurring annually is rising steadily, as a result both of aging of the world population, and of an age-specific increase in some countries [162]. Insight into the mechanism(s) by which bone loss occurs can be gained by measurement of biochemical markers of bone turnover, which reflect either osteoblast function/bone formation or osteoclast function/bone resorption. At present, bone markers are important tools in evaluating the pathogenesis and treatment of osteoporosis in clinical studies, but their utility in the management of individual patients is limited by assay variability, low predictive value for skeletal events and high cost [166]. In recent years, evidence has accrued that suggests the risk of fragility fractures is increased in both types of diabetes, albeit by different mechanisms. Hip fracture is the only fracture type evaluable in these analyses, because of the paucity of studies of other fracture types. Meta-analyses of these observational studies report increased risk of all fractures, and also those of the hip, forearm and foot (Figure 48. A second mechanism by which skeletal fragility is likely to be increased is via an increased propensity to falls as a result of disease complications. Neuropathy, visual impairment, cerebrovascular disease and hypoglycemia in particular are likely to increase falls risk. In the only study to date that has evaluated this 796 Bone and Rheumatic Disorders in Diabetes Chapter 48 (a) Study Forsen et al.
Diabetes-specific quality of life the use of diabetes-specific quality of life measures leads to similar conclusions [104] 400 medications order lithium 150mg otc. When evaluated with either a generic pediatric quality of life measure [111] or with disease-specific questions symptoms 8 dpo purchase 150mg lithium with visa, adolescents reported a relatively good quality of life which was only moderately affected by their diabetes medicine urology buy 150 mg lithium overnight delivery, yet there was a great deal of inter-individual variation in response [112] medicine to stop runny nose generic lithium 300mg on-line. Differences in metabolic control or other biomedical or psychosocial factors may be responsible for this variability medicine naproxen lithium 150 mg with visa, although there is little consistency across studies medications when pregnant buy lithium 150mg line. For example, improved metabolic control has sometimes [113], but not invariably [112], been found to be associated with better diabetes quality of life in adolescents. These relationships occur regardless of type of treatment (conventional or intensive insulin therapy) [31], or type of diabetes-associated quality of life measures employed [115]. More recent studies evaluating changes in quality of life associated with the use of continuous subcutaneous insulin infusion have been mixed, with some indicating no benefit, while others suggesting modest benefit [117], particularly amongst children and their parents [118]. Those authors suggest that individuals diagnosed earlier in development may be more adept at integrating the disease as part of their lifestyle and thus find less disruption from diabetes later in life. More recent work also suggests that the linkages between marital satisfaction, higher levels of diabetes-related satisfaction and better metabolic control may reflect better psychosocial adaptation to a variety of illness-related and marital role stresses and strains [120]. Group therapy programs, which are far more common, have similarly shown either very small positive effects or no reduction in distress. A major focus for such groups, at least early on, is to provide participants with more medical information about diabetes [130,132]. Over time, participants become more comfortable in discussing personal concerns, diabetes-related and otherwise. The broad range of topics discussed may include coming to terms with unfinished grieving over diabetes-associated problems, dealing with guilt that they may have caused their own complications and coping with fears about loss of independence [133]. As with individual psychotherapy, the efficacy of formal group therapy, in terms of improved mood or metabolic control, has not been studied extensively in large, carefully designed studies [134] and the quality of the current research is considered "weak" from a methodologic perspective [128]. Anecdotal reports suggest that many participants leave the group happier, or better adjusted, and various "curative factors" have been identified by patients as being a major benefit of group therapy, including interpersonal learning, the experience of catharsis, development of insight into problems and an understanding that the individual is not alone in experiencing disease-related psychologic distress [135,136], but analyses of outcomes from formal clinical trials with children and adults with diabetes have been less sanguine [126,128,137]. Interventions to reduce psychologic distress Traditional psychotherapy Individual or group psychotherapy or supportive counseling should be as effective in children or adults with diabetes as in individuals without diabetes but with similarly high levels of psychologic distress [124]. Traditional individualized and group therapy has been used to provide emotional support for both children and adults with diabetes, and may be particularly beneficial for patients who are confronting the development of complications such as blindness [129,130]. Studies of individual psychotherapeutic interventions are rare, but data from a single, very small randomized trial are quite promising. In neither group were there meaningful changes in glycemic control at 6 or 12 months after therapy initiation, but both were equally effective in lowering depressive symptoms to a modest degree 814 Psychologic Factors and Diabetes Chapter 49 [140]. Although hypoglycemia can never be considered to be entirely benign, it may have a relatively small role in the etiology of neurocognitive changes in patients with diabetes [148,149]. Pharmacotherapy Diabetes-related depression and anxiety disorders have also been treated successfully with pharmacotherapy [141,142]. These different psychoactive drug classes differentially affect metabolic control. Nortriptyline produces a sustained increase in HbA1c values; in contrast, both fluoxetine and alprazolam reduce HbA1c values significantly. The physiologic basis for these differential effects remains unknown, but most experts believe that pharmcotherapy-induced hyperglycemia can be handled readily with appropriate adjustments to the diabetes management regimen [146]. All subjects were followed for a median of 52 months, and only mortality outcomes were reported. There was a significant reduction in all cause mortality, but only for those depressed patients with diabetes who received this simple depression management strategy, demonstrating that even minimal management of depression can have salutary effects in the health of older adults with diabetes. In contrast, those diagnosed after that early "critical period" show very mild cognitive dysfunction which is limited primarily to measures of overall intelligence and to performance on speeded tasks, particularly those having a visuoperceptual component [156]. Learning, memory and problem-solving skills are largely intact in this "later onset" patient population, or are only very minimally [157] and inconsistently affected [158,159]. Regardless of age at diagnosis, children with diabetes also tend to achieve lower scores than their peers without diabetes on measures of academic achievement [157,160], and have somewhat poorer grades in school [161], with these latter effects especially pronounced in children with a very early onset of diabetes [162]. The magnitude of the cognitive dysfunction seen in children with diabetes tends to be quite modest, as demonstrated by a formal meta-analysis of 19 pediatric studies encompassing 1393 children with diabetes and 731 healthy comparison subjects. In contrast, effect sizes were more than twice as large when comparing early-onset subjects with diabetes with their peers without diabetes [156]. Using clinical rather than statistical criteria, one similarly finds marked differences between children with an early, as compared with a later, onset of diabetes. One large study found that 24% of children with an early onset of diabetes meet criteria for clinically significant impairment, as compared with only 6% of children with a later onset of diabetes, and 6% of a comparison group without diabetes [153]. This age at onset phenomenon has also been reported in adults diagnosed with diabetes early in life. In the largest longest prospective pediatric study to date, a representative sample of 90 newly diagnosed youngsters with diabetes and 84 healthy children drawn from the community have been followed over a 12-year period. No between-group differences were evident at study entry [165] but, 2 years later, those children diagnosed before age 4 manifested developmental delays in so far as their scores on both the Wechsler Vocabulary and Block Design subtests improved less over time, relative to either children with a later diabetes onset or to community control subjects [166]. Children with an early age at onset were particularly affected, and performed significantly worse on measures of attention and executive function than those with a somewhat later onset of diabetes [151]. For example, no changes in neuronal morphology were found in very young (1 month old) rats despite recurrent bouts of experimentally induced severe hypoglycemia, whereas 2 months of insulin-controlled diabetes caused a reduction in dendritic branching and fewer dendritic spines on neurons, and this was associated with poorer performance on measures of spatial memory [174]. These findings suggest that hypoglycemia is unlikely to be sufficient to induce significant brain dysfunction in most children, at least in those diagnosed with diabetes after the age of 7 years; however, for children with an early onset of diabetes, hypoglycemia may have a contributory role in the development of brain dysfunction [154,159]. Effects of hypoglycemic episodes on brain function Hypoglycemia has long been considered to be the cause of these neuropsychologic deficits, particularly in children with an early onset of diabetes [153,155]. Not only are rates of severe hypoglycemia significantly higher in children younger than 5 years of age, compared with children older than 5 (48% vs 13%), but hypoglycemia is also more likely to reccur in this younger group [169]. Behavioral factors could also contribute to the high rates of hypoglycemia early in life. Falling blood glucose levels may go unrecognized and untreated because very young children cannot adequately communicate that they are developing hypoglycemic symptoms. Although that view seems quite plausible, recent large well-designed cross-sectional [164,170] and longitudinal [171,172] studies completely failed to find any relationship between recurrent episodes of hypoglycemia and cognitive impairment, whereas others have reported only very weak and inconsistent findings [159] or have data sets in which severe hypoglycemia and age at onset tend to be confounded [173]. Similarly, both animal neuropathology [174] and human neuroimaging studies [167,175,176] are consistent with that view. Compared with their peers without diabetes, adolescents with diabetes in good metabolic control showed significant increases in delta and theta (slow wave) activity, significant declines in alpha peak frequency in frontal brain regions, and declines in alpha, beta and gamma fast wave activity in posterior temporal regions [177]. Both earlier age of diabetes onset and episodes of severe hypoglycemia were strong predictors of abnormality in that study, as well as in several earlier studies [179]. When auditory or visual evoked potentials were recorded, children and adolescents with a 2 years or more history of diabetes showed significant neural slowing, as evidenced by increased latencies, whereas those with less than 2 years of diabetes had normal latencies [180]. The greatest reductions in brain perfusion were found in the basal ganglia and frontal regions, followed by parietal and temporal areas. The extent to which these cerebrovascular changes contribute to cognitive dysfunction remains to be determined. Within this cohort, 16% manifested this anomaly compared to less than 1% of the general pediatric population [175]. These anomalies apparently developed within a relatively brief period of time (mean duration of diabetes in this sample was approximately 7 years), and were unrelated to a past history of hypoglycemia. By contrast, children who experienced 816 Psychologic Factors and Diabetes Chapter 49 one or more episodes of severe hypoglycemia (seizure or coma) had smaller gray matter volumes than those with no such history (724 vs 764 cm3), regardless of whether the hypoglycemic event occurred early in life or at a somewhat later age. Total brain volume was comparable in the two groups, but those children with diabetes who experienced one or more episodes of severe hypoglycemia had a slight reduction in gray matter in the left (but not right) temporal occipital region. This pattern of highly circumscribed effects, localized primarily to the left hemisphere, is consistent with what has been reported in adults with a long history of childhood-onset diabetes [183], as well as in several case reports [184]. Lifetime HbA1c values, used to estimate of chronic hyperglycemia, were associated with less cortical volume in the right posterior brain regions (particularly the right cuneus and precuneus), also replicating findings in adults with diabetes [183]. Chronic hyperglycemia was also associated with less white matter, and these effects were most pronounced in parietal brain regions. Even when differences were detected, they were modest at best, with effect sizes (d) ranging from 0. Moreover, with only one exception ("crystallized intelligence"), virtually all of the cognitive tasks on which patients with diabetes perform more poorly were those that also required rapid responding. Remarkably, the magnitude of the cognitive differences found in these older adults was similar (d = 0. Multiple studies have also demonstrated that cerebral blood flow patterns are abnormal in adults with diabetes, with these effects greatest in frontal and frontotemporal brain regions [197]. In one large study, 85% of middle-aged adults with diabetes showed hypoperfusion in one or more region of interest compared to 10% of controls; similarly, 58% of subjects with diabetes showed hyperperfusion, compared to 20% of controls [182]. Compared with a group of healthy individuals without diabetes, young adults with a childhood onset of diabetes manifested significantly less gray matter (approximately 5%) in the right superior temporal gyrus, and in several left hemisphere regions, including the temporal gyrus, angular gyrus, medial frontal gyrus, inferior parietal lobule and thalamus [183]. These structures are especially important for attention, memory and language processing. The strongest predictor of gray matter density reduction was degree of chronic hyperglycemia in so far as higher lifetime HbA1c values were consistently correlated with lower gray matter density. Reductions in white matter volume have also been noted, with effects being greatest amongst adults with a longer history of chronic hyperglycemia and microvascular complications [199]. Subjects who had clinically significant proliferative diabetic retinopathy at study entry, or who developed retinopathy during the course of the follow-up period, showed a significant decline in psychomotor efficiency, compared to demographically similar subjects without diabetes. In contrast, those without retinopathy at either time showed no evidence of psychomotor slowing. The risk of cognitive change was predicted by four variables: the presence or development of proliferative retinopathy, the presence of autonomic neuropathy, elevated systolic blood pressure and longer duration of diabetes. The resulting statistical model identified, with 83% accuracy, subjects who showed significant cognitive decline and explained 53% of the variance. Other microvascular complications, particularly peripheral neuropathy, are also associated with changes in brain function and structure [177,193,196,203,204]. Because middle-aged adults without diabetes who have retinal microaneurysms also show a pattern of cognitive decline that is characterized by psychomotor slowing [205], it has been suggested that retinopathy may serve as a general marker of cerebral microangiopathy [148,206]. This is quite plausible, given the well-known homology between the retinal and cerebral microvascular systems [207]. In patients with clinically significant diabetic retinopathy, the resulting microangiopathy could lead to cerebral hypoperfusion and thereby contribute to the development of abnormalities in brain structure and function by interfering with the efficient delivery of glucose and other key substances to neural tissue [148,198]. The relationship often reported between peripheral neuropathy and brain dysfunction in patients with diabetes may simply reflect the fact that microvascular complications tend to appear contemporaneously and have a common origin [208,209]. That is, microvascular disease may be the primary mechanism underlying the development of neurocognitive dysfunction in young and middle-aged adults [150]. Repeated episodes of severe hypoglycemia and cognitive dysfunction the widespread belief that moderately severe hypoglycemia will induce cognitive impairment in adults with diabetes appears to have little support from a growing body of research on this topic. Lifetime rates of severe hypoglycemia, defined as including a seizure or coma, were high, with a total of 1355 episodes reported in 453 subjects over the course of the study. Despite that, no relationship whatsoever was found between the cumulative number of severe hypoglycemic episodes and performance on a comprehensive battery of cognitive tests [210]. Cross-sectional studies have also failed to find robust relationships between cognition and episodes of severe hypoglycemia [186,201]. Several earlier studies did note a link between hypoglycemia and brain damage [211], but all relied on small samples of highly selected subjects who were assessed with a limited number of cognitive tests which yielded a pattern of results that was not entirely consistent with brain damage. For example, subjects with repeated hypoglycemia performed slower, but no less accurately, on a number of tests, and earned somewhat lower scores on the Performance subtests of the Wechsler Adult Intelligence Scale, yet learning and memory skills were intact. This latter finding is unexpected because of the well-known associations between memory and the hippocampus, a major focus of structural damage following profound hypoglycemia in rodents [212], nonhuman primates [213] and humans [184,214]. Whether moderately severe bouts of hypoglycemia adversely affect brain structure 818 Psychologic Factors and Diabetes Chapter 49 remains controversial, with some [215] but not all [174] studies finding evidence of neuronal necrosis in rodent models. In human studies it can be quite difficult to make attributions specifically to hypoglycemia, rather than to chronic hyperglycemia, because patients who experience hypoglycemia also have a history of poor metabolic control [177]. As described in Chapter 33, severe and profound hypoglycemia can induce significant structural and function brain damage, but the prevalence of this phenomenon in adults with diabetes seems extremely low. Several recent studies and review articles have noted an increased risk of dementia that ranges 1. The degree of chronic hyperglycemia, as indexed by HbA1c levels, is the best (albeit imperfect) predictor of impairment in the older patient with diabetes, although a growing body of research has identified other diabetes-related conditions, including hyperinsulinemia [239,240], hypertension [220] and hypercholesterolemia [241].
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