Rejected

Intractable neuropathic pain is a frequent consequence of nerve injury or disease. When peripheral nerves are injured, damaged axons undergo Wallerian degeneration. Schwann cells, mast cells, fibroblasts, keratinocytes and epithelial cells are activated leading to the generation of an "inflammatory soup" containing cytokines, chemokines and growth factors. These primary mediators sensitize sensory nerve endings, attract macrophages, neutrophils and lymphocytes, alter gene expression, promote post-translational modification of proteins, and alter ion channel function in primary afferent neurons. This leads to increased excitability and spontaneous activity and the generation of secondary mediators including colony stimulating factor 1 (CSF-1), chemokine C-C motif ligand 21 (CCL-21), Wnt3a, and Wnt5a. Release of these mediators from primary afferent neurons alters the properties of spinal microglial cells causing them to release tertiary mediators, in many situations ATP-dependent mechanisms. Tertiary mediators such as BDNF, tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and other Wnt ligands facilitate the generation and transmission of nociceptive information by increasing excitatory glutamatergic transmission and attenuating inhibitory GABA and glycinergic transmission in the spinal dorsal horn. This review focusses on activation of microglia by secondary mediators, release of tertiary mediators from microglia and a description of their actions in the spinal dorsal horn. Attention is drawn to the substantial differences in the precise roles of various mediators in males compared to females. At least 25 different mediators have been identified but the similarity of their actions at sensory nerve endings, in the dorsal root ganglia and in the spinal cord means there is considerable redundancy in the available mechanisms. Despite this, behavioral studies show that interruption of the actions of any single mediator can relieve signs of pain in experimental animals. We draw attention this paradox. It is difficult to explain how inactivation of one mediator can relieve pain when so many parallel pathways are available.

This study aims to compare the success rate of thoracic paravertebral block (TPVB) and the effect of postoperative analgesia between two approaches.

Although sibling sexual abuse (SSA) may be the most common type of intrafamilial sexual abuse, it has not been widely studied. The lack of studies makes it very difficult for clinicians to create a comprehensive framework about this complex phenomenon, particularly in comparison with other forms of intrafamilial sexual abuse, such as father-daughter incest. SSA is still underrecognized and underdisclosed but it has the potential to be every bit as harmful as sexual abuse by a parent. The topic rarely finds its way into the more general psychiatry or social work literature. It is imperative to increase healthcare practitioners' awareness of this complex subject to improve their ability to listen to, detect, and manage the disclosures of SSA in adolescent populations. This paper presents vignettes of three 13-to-15-year-old adolescent girls who disclosed SSA during inpatient hospitalization in an adolescent psychiatric and medicine department. These cases illustrate the complexity of SSA, which has been associated with a wide spectrum of both mental and physical symptoms. Adolescent victims of SSA experience serious distress, with various and numerous psychiatric manifestations, including but not limited to depression and suicide attempts, addictive behaviors, post-traumatic stress symptoms, and eating disorders. Physical symptoms should also alert practitioners: adolescent survivors are more likely to be affected by somatic complications such as sexually transmitted diseases, chronic pain, urogenital symptoms, and nutritional disorders. We offer some recommendations to improve the detection and support of distressed adolescents disclosing SSA. Listening to them and offering a protective multidisciplinary response can limit the lasting damage and contribute to the repair process.

Several factors can contribute to the development and chronification of migraines, including stress, which is undoubtedly a major trigger. Beyond pharmacotherapy, other treatment methods also exist, including behavioral techniques aiming at reducing patients' stress response. However, the exact brain mechanisms underlying the efficacy of such methods are poorly understood. Our pilot study examined whether the regular practice of autogenic training (AT) induces functional brain changes and if so, how it could be associated with the improvement of migraine parameters. By exploring neural changes through which AT exerts its effect, we can get closer to the pathomechanism of migraine. In particular, we investigated the effect of a headache-specific AT on brain activation using an implicit face emotion processing functional MRI (fMRI) task in female subjects with and without episodic migraine. Our focus was on migraine- and psychological stress-related brain regions. After a 16-week training course, migraineurs showed decreased activation in the migraine-associated dorsal pons to fearful compared with neutral visual stimuli. We also detected decreasing differences in supplementary motor area (SMA) activation to fearful stimuli, and in posterior insula activation to happy stimuli between healthy subjects and migraineurs. Furthermore, migraineurs reported significantly less migraine attacks. These brain activation changes suggest that AT may influence the activity of brain regions responsible for emotion perception, emotional and motor response integration, as well as cognitive control, while also being able to diminish the activation of regions that have an active role in migraine attacks. Improvements induced by the training and the underlying neurophysiological mechanisms are additional arguments in favor of evidence-based personalized behavioral therapies.

Trigeminal neuralgia (TN) is a debilitating neuropathic pain involving the fifth cranial nerve. There has been no study investigating the clinical and socioeconomical characteristics of patients with TN in Indonesia. A total of 100 patients were included in this study. Symptoms indicating a later stage of the illness, namely, involvement of all the trigeminal nerve branches, numbness, and concomitant persistent pain, were the common presentations found in our cohort. Only one TN diagnosis was made by a general practitioner (GP). None were immediately referred to a neurosurgeon following their diagnosis. Access to our clinic took as long as 4.7 ± 5.1 years (mean ± SD) from the onset. Older age was a significant predictor of an increased likelihood of not knowing their illness upon the referral (21.9%, = 0.008). Upon their first presentation, 25.5% of patients had experienced drug-related side effects due to prolonged medication. Only 50% of patients were compensated by the universal health coverage (UHC) system. Seven patients spent ≥ 50 million rupiahs and eight patients had already lost their jobs. In conclusion, early contact with a neurosurgeon contributes to better management of TN, both for the patients and healthcare system in Indonesia. A refined understanding of TN nature is still needed in this country.

The mitochondrial trifunctional protein (MTP) is a multienzyme complex of the fatty acid betaoxidation cycle. Mitochondrial trifunctional protein deficiency (MTPD), a rare condition that leads to failure of converting certain fats to energy is characterized by decreased activity of three enzymes in the enzyme complex. Signs and symptoms of MTPD may present during infancy or later in life; those that begin after infancy include hypotonia, muscle pain, rhabdomyolysis, and peripheral neuropathy. We report a Turkish boy diagnosed with MTPD after being investigated for polyneuropathy of unknown origin since infancy.

P2X receptors (P2XRs) are trimeric, non-selective cation channels activated by extracellular ATP and widely distributed in the digestive system. P2XRs have an important role in the physiological function of the digestive system, such as neurotransmission, ion transports, proliferation and apoptosis, muscle contraction, and relaxation. P2XRs can be involved in pain mechanisms both centrally and in the periphery and confirmed the association of P2XRs with visceral pain. In the periphery, ATP can be released as a result of tissue injury, visceral distension, or sympathetic activation and can excite nociceptive primary afferents by acting at homomeric P2X(3)R or heteromeric P2X(2/3)R. Thus, peripheral P2XRs, and homomeric P2X(3) and/or heteromeric P2X(2/3)R in particular, constitute attractive targets for analgesic drugs. Recently studies have shown that P2XRs have made significant advances in inflammation and cancer. P2X7R mediates NLRP3 inflammasome activation, cytokine and chemokine release, T lymphocyte survival and differentiation, transcription factor activation, and cell death. The P2X7R is a potent stimulant of inflammation and immunity and a promoter of cancer cell growth. This makes P2X7R an appealing target for anti-inflammatory and anti-cancer therapy. It is believed that with the further study of P2XRs and its subtypes, P2XRs and its specific antagonists will be expected to be widely used in the treatment of human digestive diseases in the future.

Thrombocytopenia as a precipitating factor for pituitary apoplexy (PA) is very rare event. There are only five reported cases of PA secondary to thrombocytopenia caused by underlying haematological malignancy. Herein, we report a case of 60-year-old male presenting with acute-onset headache, bilateral vision loss, and ptosis. Computed tomography and magnetic resonance imaging revealed findings indicative of pituitary adenoma with apoplexy. He was noted to have thrombocytopenia, and bone marrow evaluation revealed precursor B-lineage CALLA-positive acute lymphoblastic leukemia. Accordingly, he was started on dexamethasone and vincristine but succumbed to -related hospital-acquired pneumonia two weeks after initiation of chemotherapy. We performed a literature search and found five cases of pituitary apoplexy secondary to haematological malignancy-related thrombocytopenia. The usual age of presentation was in the 6 to 7 decade, and there was slight male preponderance. The underlying pituitary adenoma was either nonfunctioning or a prolactinoma, and in majority, the apoplexy event occurred after the diagnosis of haematological malignancy. The platelet counts at the time of PA were less than 30 × 10/L in all, and the malignancy subtypes were acute or chronic myeloid leukemia and chronic lymphoid leukemia. The current case highlights the importance of careful evaluation for the cause of thrombocytopenia in a case of PA.

Several case reports have illustrated a rare neurological manifestation, idiopathic intracranial hypertension (IIH), in patients with thyrotoxicosis. However, none were diagnosed with thyroiditis. We report the case of a patient with subacute thyroiditis who presented with severe intractable headache due to IIH. . A 36-year-old woman visited Lampang Hospital in February 2021 complaining of neck pain and progressive severe intractable headache. Her vital signs and neurological examination were normal. Thyroid examination revealed a single 1 cm right thyroid nodule. A computed tomography (CT) scan of her brain illustrated diffuse brain edema. However, CT angiography and venography of the brain did not show abnormalities. The opening pressure of the cerebrospinal fluid was elevated (27 cmHO). The free triiodothyronine level was 6.19 pg/mL, free thyroxine was 2.32 ng/dL, and thyroid-stimulating hormone was 0.0083 IU/mL. Anti-Tg was positive at a low titer, but anti-TPO was negative. TRAb was also negative. Methimazole and acetazolamide were prescribed and monitored. The symptoms resolved completely within 2 weeks of onset. Thyroid hormones had returned to normal by 8 weeks.