Dual wavelength 5-aminolevulinic acid photodynamic therapy using a novel flexible light-emitting diode unit

Background

Photosensitizers used for photodynamic therapy (PDT) to treat dermatologic disease are metabolized into mainly protoporphyrin IX (PpIX), which has five absorption wavelength peaks: 410?nm, 510?nm, 545?nm, 580?nm, and 630?nm. Although only red light around 635?nm and blue light around 400?nm are used as light sources for PDT, the efficiency of PDT might be improved by using multiple wavelengths, including those that correspond to the other absorption peaks of PpIX. Furthermore, because the target disease often occurs on the face, a flexible-type light-source unit that can be fitted to the lesion without unnecessarily exposing the mucous membranes, e.g., the eyes, nostrils, and mouth, is preferred.

An updated review on pathophysiology and management of burning mouth syndrome with endocrinological,psychological and neuropathic perspectives

Burning mouth syndrome (BMS) is a chronic oro‐facial pain disorder of unknown cause. It is more common in peri‐ and post‐menopausal women, and sex hormone dysregulation is believed to be an important causative factor. Psychosocial events often trigger or exacerbate symptoms, and persons with BMS appear to be predisposed towards anxiety and depression. Atrophy of small nerve fibres in the tongue epithelium has been reported, and potential neuropathic mechanisms for BMS are now widely investigated. Historically, BMS was thought to comprise endocrinological, psychosocial and neuropathic components. Neuroprotective steroids and glial cell line–derived neurotrophic factor family ligands may have pivotal roles in the peripheral mechanisms associated with atrophy of small nerve fibres. Denervation of chorda tympani nerve fibres that innervate fungiform buds leads to alternative trigeminal innervation, which results in dysgeusia and burning pain when eating hot foods. With regard to the central mechanism of BMS, depletion of neuroprotective steroids alters the brain network–related mood and pain modulation. Peripheral mechanistic studies support the use of topical clonazepam and capsaicin for the management of BMS, and some evidence supports the use of cognitive behavioural therapy. Hormone replacement therapy may address the causes of BMS, although adverse effects prevent its use as a first‐line treatment. Selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs) may have important benefits, and well‐designed controlled studies are expected. Other treatment options to be investigated include brain stimulation and TSPO (translocator protein 18 kDa) ligands.     

Psychiatric symptoms associated with oculogyric crisis: a review of literature for the characterization of antipsychotic-induced episodes.

Antipsychotics have been found to induce recurrent psychotic episodes lasting minutes to hours, mostly accompanied by oculogyric crisis (OGC). To characterize this side effect, antipsychotic-induced and postencephalitic OGCs that were reported in the literature were compared to find out common characteristics of OGCs and their associated symptoms. Both postencephalitic and antipsychotic-induced OGCs were found to occur late in the day and at regular intervals, and were associated with autonomic symptoms such as profuse sweating, facial flushing, transitory hypertension and difficulty in micturition. They were often associated also with transient psychiatric episodes: visual hallucinations and illusions, auditory hallucinations, delusions, catatonic phenomena, obsessive thoughts and panic attacks. These (OGC) characteristics will be useful in recognizing antipsychotic-induced psychiatric episodes. The associated psychiatric episodes were noted to recur occasionally also without OGC in a few postencephalic cases, and during gradual dose reduction or after a switch to a novel or low-potency antipsychotic in drug-induced cases. These findings suggest that episodes with the OGC characteristics but without OGC per se, may be less severe reactions to antipsychotic medication than those with OGC, and may represent manifestations of subclinical OGC.