Screening for the loss of protective sensation in people without a history of diabetic foot ulceration: Validation of two simple tests in India.

The ability of the Ipswich touch test (IpTT) and VibratipTM to detect loss of protective sensation (LOPS) was tested against a neurothesiometer in an outpatient diabetic population without a history for ulceration. Our results support the use of the IpTT as a screening tool for LOPS, but not of VibratipTM.

Undiagnosed severe sleep apnoea and diabetic foot ulceration - a case series based hypothesis: a hitherto under emphasized factor in failure to heal.

BACKGROUND: Although great progress has been made in managing diabetic foot disease, it continues to carry significant morbidity and mortality. Obstructive sleep apnoea (OSA) and diabetes frequently coexist and recent studies suggest significant under-recognition of OSA in those with diabetes. There are no current reports on the direct clinical impact of OSA on acute or chronic diabetic foot ulcer healing. CASE REPORT: We describe three cases with Type 2 diabetes and a mean BMI of 50 kg/m(2) in whom we believe undiagnosed severe OSA may have impeded the rate of recovery of acutely infected foot ulcers. Despite standard care whilst in hospital with optimization of glycaemia, daily wound care, ulcer offloading techniques including casting, it was difficult to achieve satisfactory granulation in the first two cases with previously unrecognized and hence untreated severe OSA (Apnoea-Hypopnea Index > 30) until correction had been achieved through continuous positive airway pressure therapy (CPAP). In the third case, despite all optimization techniques, healing has not been achieved and individuals' reluctance to consider CPAP may be one possible factor. DISCUSSION: We observe in three severely obese individuals with diabetes that untreated severe OSA may have contributed to delayed wound healing. We also observed an improvement in two individuals after institution of CPAP therapy. Clinicians managing the diabetic foot should consider investigating the presence of OSA in non-healing or slowly progressive foot ulcers when all other factors have been fully optimized.

[Life paths and motifs. Meeting points of hypnotherapy and music therapy]. / Sorsok és motivumok. A hipnoterápia és a zeneterápia érintkezési pontjai.

Effects both of hypnotherapy and music therapy are originated from an attunement as supposed by the author. Either to a hypnotherapist's suggestions or to a piece of music one is able to be tuned in them. On one hand, the hypnotherapist's prosody, which can be called as melodic declamation seen as a musical phenomenon transmitting emotions. On the other hand, music has got emotional and visceral impacts. As a meeting points of these two methods four possibilities are shown by the author: 1. musical analogies of vitality affects ; 2. paternal and maternal archetypes in music; 3. analogies of copings in music; 4. corrections of psychological deficits by virtue of hypno- and music therapy with parallel used energy healing method. Finally, the author suggests, that hypnosis is regarded as an inductive method expressing its effect from outside to inside; music, however is likely to be employed as a deductive therapeutic tool, effecting from inside to outside.

[Body-mind unity in tandem hypnotherapy]. / Test-lélek egység a tandem hipnoterában.

INTRODUCTION: The new bodymind theory describes unity of body and mind as a quantum process, which can go back to embryonic period of life. METHOD: Authors have worked out tandem hypnotherapy method regarding bodymind theory. Tandem has two meanings: (1) a multi-seater bicycle, (2) a mosaic word: Touch of Ancient and New generations with a Dialogue Experiencing Oneness of Minds (TANDEM). Hypnotherapy, psychodrama, family therapy, Hellinger's systemic-phenomenological approach, and, the holding-therapy can be viewed as precedents of the method. More than two persons in a physical closeness touching each other take part in therapy: (1) patient(s), (2) one or more co-therapists; one or more antagonists (in the latter case is of hypnodrama), (3) therapist, who is responsible to take the tandem of patient(s) and co-therapist(s) to trance, while (s)he keeps distance securing neutrality. RESULTS: The method will be illustrated with some case-vignettes. DISCUSSION: Sensory-motor level of development is supposed by the authors as stemmed from fetal period of life. It is suggested to be paralled to associative mode of experiencing, in which object and subject can't be viewed as differenciated from each other resulting unity or oneness experience. The most effective stimulus of associative mode of experiencing is regarded to be physical closeness and touching, which are seen in intimate situations. That is the reason why fundamental rules of therapeutic touching are to be kept. CONCLUSION: The new method can be viewed as a form of bodypsychotherapy having possibilities to resolve pathological consequences of either fetal or intergenerational traumas.

Small fibre dysfunction, microvascular complications and glycaemic control in type 1 diabetes: a case-control study.

AIMS/HYPOTHESIS: The aim of this study was to determine the influence of microvascular disease on C-fibre function in patients with type 1 diabetes of moderate duration. METHODS: The axon-reflex flare area induced on the dorsum of the foot by local skin heating to 47 °C was measured with a laser Doppler imager (LDI) in sex-, age- and height-matched groups with type 1 diabetes, with and without microvascular disease (MV+ and MV-, respectively) and in healthy controls (HC). Each group consisted of 24 individuals and all were free from clinical neuropathy (neuropathy disability score <3 and Toronto clinical neuropathy score <5). RESULTS: LDI flare (LDIflare) was reduced in MV+ compared with HC (5.1 ± 1.8 vs 10.0 ± 3.1 cm², p < 0.0001) and MV- groups (9.9 ± 2.9 cm², p < 0.0001). MV- and HC groups did not differ. There was no difference in diabetes duration between MV- and MV+ groups (17.5 ± 5.7 and 20.1 ± 5.2 years, p = 0.21) nor current HbA(1c) (MV- 8.0 ± 1.2% [64 ± 10 mmol/mol]; MV+ 8.0 ± 0.9% [64 ± 9 mmol/mol], p = 0.53); neither variable correlated with flare size. In contrast, duration-averaged HbA(1c) was higher in the MV+ group (8.6 ± 0.9% [70 ± 9 mmol/mol] vs 7.6 ± 0.6% [60 ± 7 mmol/mol], p < 0.001) and correlated with LDIflare size (r = -0.50, p < 0.001). Triacylglycerols were higher in MV+ compared with MV- (1.23 ± 0.121 vs 0.93 ± 0.7 mmol/l, p = 0.04), but other metabolic variables did not differ between the groups. CONCLUSIONS/INTERPRETATION: We have shown that glycaemic burden and the presence of microvascular complications are associated with small fibre dysfunction in type 1 diabetes.

Seizures and reduced life span in mice lacking the potassium channel subunit Kv1.2, but hypoexcitability and enlarged Kv1 currents in auditory neurons.

Genes Kcna1 and Kcna2 code for the voltage-dependent potassium channel subunits Kv1.1 and Kv1.2, which are coexpressed in large axons and commonly present within the same tetramers. Both contribute to the low-voltage-activated potassium current I Kv1, which powerfully limits excitability and facilitates temporally precise transmission of information, e.g., in auditory neurons of the medial nucleus of the trapezoid body (MNTB). Kcna1-null mice lacking Kv1.1 exhibited seizure susceptibility and hyperexcitability in axons and MNTB neurons, which also had reduced I Kv1. To explore whether a lack of Kv1.2 would cause a similar phenotype, we created and characterized Kcna2-null mice (-/-). The -/- mice exhibited increased seizure susceptibility compared with their +/+ and +/- littermates, as early as P14. The mRNA for Kv1.1 and Kv1.2 increased strongly in +/+ brain stems between P7 and P14, suggesting the increasing importance of these subunits for limiting excitability. Surprisingly, MNTB neurons in brain stem slices from -/- and +/- mice were hypoexcitable despite their Kcna2 deficit, and voltage-clamped -/- MNTB neurons had enlarged I Kv1. This contrasts strikingly with the Kcna1-null MNTB phenotype. Toxin block experiments on MNTB neurons suggested Kv1.2 was present in every +/+ Kv1 channel, about 60% of +/- Kv1 channels, and no -/- Kv1 channels. Kv1 channels lacking Kv1.2 activated at abnormally negative potentials, which may explain why MNTB neurons with larger proportions of such channels had larger I Kv1. If channel voltage dependence is determined by how many Kv1.2 subunits each contains, neurons might be able to fine-tune their excitability by adjusting the Kv1.1:Kv1.2 balance rather than altering Kv1 channel density.