Les douleurs périnéales chroniques

Chronic perineal pain must be approached by clinical process of elimination, based on ruling out local pathological lesions. In the absence of any visible cause, perineal pain may be related to a somatic nerve disorder of vegetative or musculoligamentary origin. The pudendal nerve is the main nerve in the perineum. Pudendal neuralgia is usually related to pudendal canal syndrome, caused either by entrapment between ligaments (sacrotuberous or sacrospinous ligaments) or by aponeuralgia (aponeuralgia of the internal obturator or of Alcock’s canal). The symptoms include positional perineal pain (aggravated when sitting) that is not sufficient to regularly wake the patient at night and is not associated with any objective sensory disorder. Nerve blocks confirm the diagnosis (Nantes criteria). Treatment can be through drugs for neuropathic pain, infiltrations and surgical nerve release. Entrapment of the ilio-inguinal or genito-femoral nerves is generally subsequent to pelvic surgery. In cases located in proximity to the abdomino-pelvic wall, an anaesthetic injection loco dolenti is easy to administer for diagnosis and treatment, with the addition of local cortico-steroids. Pain caused by the vegetative and sympathetic systems is much more diffuse than somatic neuropathic pain. Vulvar vestibulitis causes hypersensitivity of the vulva, making any contact, in particular sexual activity, unbearable. The mechanism is still unclear and treatment is purely symptomatic. Testicular pain can suggest post-operative nerve impairment, but the most frequent cause of chronic testicular pain, in the absence of any local lesions, is due to projected pain caused by minor intervertebral displacement in the thoraco-lumbar joint, which can be treated with manipulation, physiotherapy or injection. Musculoskeletal pain may include projected thoracolumbar pain and myofascial pain, which may be part of a wider context of fibromyalgia. Paroxysmal pain can suggest perfectly harmless pathologies, such as proctalgia fugax (occurring once a month and lasting an average of 15 minutes) or may possibly be caused by neurological tumours (sudden shooting pains) and a pelvic and lumbar sacral MRI scan should therefore ensue. Chronic perineal pain has a significant emotional effect, making semiological analysis more complicated. This emotional component is often a result of the chronic pain, but prior physical or sexual stress factors should not be ruled out when considering psycho-behavioural management. The complexity and multidimensional nature of chronic perineal pain require a multidisciplinary approach.     

Hypertension and dementia

The increase in life expectancy is associated with a sharp rise in cognitive disorders, particularly after the age of 80 years. The identification and management of risk factors for these invalidating and distressing conditions must be considered a priority. The fact that antihypertensive treatment has been demonstrated to decrease that risk offers a new opportunity to reduce the prevalence of such related disorders and promote healthy aging.     

Electronic tracking system and wandering in Alzheimer's disease: A case study

IntroductionWandering is a behavioural disorder, which occurs in Alzheimer's disease or other dementia. People who wander are at risk of physical harm and untimely death. Moreover, wandering behaviour causes a lot of stress to the caregivers. In the last few years, different geolocation devices have been developed in order to minimise risk and manage unsafe wandering. These detection systems rarely meet patients and caregivers’ needs because they are not involved in the devices building process.AimThe aim is to explore the needs and perceptions of wandering persons and their caregivers towards existing tracking devices as well as their acceptability and usability. This paper reports a dyad case.MaterialsThe tracking system tested is presented as a mobile Global Positioning System (GPS) receiver-shaped, including function of telephony and data transfer via GSM/GPRS.MethodDyad patient/caregiver expressed their needs and perceptions towards tracking devices and gave their impressions about the functioning of the tested device at the end of the test.ResultsThe patient focused on the device's shape which he found too voluminous and unaesthetic, and was unable to give an opinion about the device's functioning. The spouse highlighted malfunctions and usage difficulties, which made the device not appropriate to her needs.ConclusionInvolving end-users in the co-design of new technologies is necessary for building tailored devices. Moreover, in this area of dementia care, the person-centred approach is essential to a tailored wandering management.     

The apolipoprotein E epsilon4 allele and the response to tacrine therapy in Alzheimer's disease.

The objective of our study was to evaluate the effects of the apolipoprotein E (ApoE) phenotype and gender on the response to tacrine treatment in Alzheimer's disease (AD). ApoE phenotyping was performed on 76 patients treated with tacrine for AD. This group comprised 33 ApoE epsilon4 allele carriers (epsilon4+) and 43 non-epsilon4 carriers (epsilon4-). Patients were treated blindly in relation to the ApoE phenotype, with incremental tacrine dosages ranging from 40 mg/day up to the highest dosage (160 mg) tolerated without side-effects. At least 6 weeks elapsed between each increase. Changes in the scores for the Alzheimer Disease Assessment Scale-Cognitive Component (ADAS-Cog) between baseline and each increment in dosage were assessed in the epsilon4- and epsilon4+ groups. The cut-off point for being considered as responsive to tacrine treatment was a 4-point decrease in the ADAS-Cog score. There was no tendency for the epsilon4- carriers to respond better than the epsilon4+ carriers. When patients were stratified by gender, no differences were found between the effects of the treatment on men and women. Consequently, these results do not support the hypothesis that the ApoE phenotype and gender are predictors of the response to tacrine in AD patients.     

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats

BACKGROUND: Neuropathic pain is inadequately treated and poorly understood at the cellular level. Because intracellular Ca signaling critically regulates diverse neuronal functions, the authors examined effects of peripheral nerve injury on the Ca transient that follows neuronal activation. METHODS: Cytoplasmic Ca levels were recorded by digital microfluorometry from dissociated dorsal root ganglion neurons of hyperalgesic animals after ligation of the fifth lumbar spinal nerve and control animals. Neurons were activated by field stimulation or by K depolarization. RESULTS: Transients in presumptively nociceptive, small, capsaicin-sensitive neurons were diminished after axotomy, whereas transient amplitude increased in axotomized nonnociceptive neurons. Axotomy diminished the upward shift in resting calcium after transient recovery. In contrast, nociceptive neurons adjacent to axotomy acquired increased duration of the transient and greater baseline shift after K activation. Transients of nonnociceptive neurons adjacent to axotomy showed no changes after injury. In nociceptive neurons from injured rats that did not develop hyperalgesia, transient amplitude and baseline offset were large after axotomy, whereas transient duration in the adjacent neurons was shorter compared with neurons excised from hyperalgesic animals, which show normalization of these features. CONCLUSIONS: A diminished Ca signal in axotomized neurons may be in part due to loss of Ca influx through voltage-gated Ca channels. The upward shift in resting Ca level after activation, which is diminished after axotomy in presumed nociceptive neurons, is a previously unrecognized aspect of neuronal plasticity. These changes in the critical Ca signal may mediate various injury-related abnormalities in Ca-dependent neuronal.     

Langerhans cell histiocytosis: therapeutic strategy and outcome in a 30‐year nationwide cohort of 1478 patients under 18 years of age

The French national cohort of children with Langerhans cell histiocytosis (LCH) has included 1478 patients since it was established in 1983. LCH therapeutic strategies substantially changed in 1998, so we have divided the cohort into two 15‐year periods. Starting in 1998, therapy duration increased from 6 to 12 months, repeated induction therapy was performed in cases showing a poor response to the first induction with vinblastine and steroids, and refractory disease in a risk organ (RO+) was treated with cladribine and cytarabine. A total of 483 (33%) patients were enrolled before 1998, and 995 (67%) after 1998. Five‐year survival was 96·6% (95% confidence interval: 95·4–97·5%) overall, improving from 92% pre‐1998 to 99% post‐1998 (P < 0·001 adjusted to disease extent). This change was supported by an increase in 5‐year survival from 60% to 92% in the RO+ group. Survival was particularly associated with cladribine and cytarabine among refractory RO+ patients. Disease reactivation was slightly less frequent after 1998, due to better enrolment of single‐system patients, extended therapy duration, and more efficient second‐line therapy. The crude rates of endocrine and neurological sequelae (the most frequent sequelae) appeared to improve over time, but this difference was not observed when the analysis was stratified by disease extent.