Risk factors for shoulder pain after stroke: A clinical study

Objectives: To investigate the risk factors for shoulder pain after stroke, and prevent its occurrence effectively. Methods: The patients with stroke treated in our hospital between September 2016 and October 2020 were reviewed retrospectively. The medical records of the included patients including age, gender, lesion side, stroke duration, hospital stay, diabetes, hypertension, heart disease, limitation of shoulder joint activity, alcohol abuse, smoking, type of stroke, Ashworth scale, Brunnstrom stage, sensory disorders, and motor arm score of National Institutes of Health Stroke Scale (NIHSS) were collected and analyzed to determine the risk factors for shoulder pain after stroke. Results: A total of 1390 patients were included based on the inclusion and exclusion criteria, consisting of 162 patients with shoulder pain after stroke and the prevalence was 11.6%. The included patients were divided into shoulder pain group and non-shoulder pain group. There were significant differences in age, stroke duration, hospital stay, diabetes, limitation of shoulder joint activity, Ashworth scale, Brunnstrom stage, sensory disorders, and motor arm score of NIHSS between the two groups (P < 0.05). Based on the multivariate regression analysis, the independent risk factors for shoulder pain after stroke included diabetes, limited shoulder joint activity, Brunnstrom grade I-III period, Ashworth 3-4 grade, motor arm score of NIHSS 3-4 points, and sensory disturbance. Conclusion: Great emphasis should be placed on the stroke patients with diabetes, limited shoulder joint activity, Brunnstrom grade I-III period, Ashworth 3-4 grade, motor arm score of NIHSS 3-4 points, or sensory disturbance, as these patients have higher risks for shoulder pain after stroke. doi: https://doi.org/10.12669/pjms.38.1.4594 How to cite this:Hao N, Zhang M, Li Y, Guo Y. Risk factors for shoulder pain after stroke: A clinical study. Pak J Med Sci. 2022;38(1):---------. doi: https://doi.org/10.12669/pjms.38.1.4594 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Rotation-hinged knee prosthesis for the treatment of Charcot arthropathy: a case report and literature review

Charcot arthropathy is a type of destructive osteoarthropathy characterized by neurotrophic and sensory disorders. The condition is relatively rare, with an insidious onset, and it is easily misdiagnosed. Total knee arthroplasty (TKA) can cause excessive joint wear, continuous inflammatory stimulation of the prosthesis, postoperative residual cavity, prosthesis loosening and subsidence, peripheral fracture, infection, and other complications. Furthermore, these complications are more likely to occur in patients with Charcot arthropathy because of disease-specific pathological characteristics, when TKA is performed. Therefore, Charcot arthropathy was once a contraindication to TKA. Recently, with the optimization of joint prostheses and the maturity of surgical techniques, more studies have reported successful cases of TKA in patients with Charcot arthropathy. We report a case of Charcot arthropathy in our hospital, and describe the patient’s medical history, clinical symptoms, signs, imaging findings, diagnosis, and the entire TKA process, to explore the TKA strategy and prosthesis selection in a patient with Charcot arthropathy.

DIAGNOSTICS OF SENSORINEURAL DISORDERS IN HAND-ARM VIBRATION SYNDROME (HAVS) - UPDATED APPROACHES

The earliest and most frequent manifestation of HAVS is limb polyneuropathy with sensory disorders. The study was conducted in order to assess the various types of sensory modality disorders by methods of functional diagnostics in HAVS. The main group of patients with an established diagnosis of HAVS and a control group of healthy individuals who have not worked in harmful and dangerous working conditions during their lives were examined. The methods of computer pallesthesiometry, quantitative sensory testing (QST) and stimulation electroneuromyography were used in the study. A comprehensive study revealed disorders of the perception of sensitivity of various modalities (vibration, pain and temperature), which indicated damage to all types of peripheral nerve structures when exposed to local vibration-unmyelinated fibers (C–type), myelinated (A-beta-type) and weakly myelinated (A-delta–type).

Reflex memory theory of acquired involuntary motor and sensory disorders

Background Explicit and implicit memories are conserved but flexible biological tools that nature uses to regulate the daily behaviors of human beings. An aberrant form of the implicit memory is presumed to exist and may be contributory to the pathophysiology of disorders such as tardive syndromes, phantom phenomena, flashback, posttraumatic stress disorders (PTSD), and related disorders. These disorders have posed significant clinical problems for both patients and physicians for centuries. All extant pathophysiological theories of these disorders have failed to provide basis for effective treatment. Objective The objective of this article is to propose an alternative pathophysiological theory that will hopefully lead to new treatment approaches. Methods The author sourced over 60 journal articles that treated topics on memory, and involuntary motor and sensory disorders, from open access journals using Google Scholar, and reviewed them and this helped in the formulation of this theory. Results From the reviews, the author thinks physical or chemical insult to the nervous system can cause defective circuit remodeling, leading to generation of a variant of implicit (automatic) memory, herein called “reflex memory” and this is encoded interoceptively to contribute to these phenomena states. Conclusion Acquired involuntary motor and sensory disorders are caused by defective circuit remodeling involving multiple neural mechanisms. Dysregulation of excitatory neurotransmitters, calcium overload, homeostatic failure, and neurotoxicity are implicated in the process. Sustained effects of these defective mechanisms are encoded interoceptively as abnormal memory in the neurons and the conscious manifestations are these disorders. Extant theories failed to recognize this possibility.

Application of Mental Nursing Care on Ny. Y With Perception Sensory Disorders: Hallucinations

Halusinasi merupakan suatu penyakit neurologis yang mempengaruhi otak yang menyebabkan timbulnya gangguan dan keanehan dalam pikiran, persepsi, emosi, gerakan dan prilaku, Halusinasi dapat di artikan suatu gangguan neurobiologis otak berat yang mempengaruhi cara berfikir, kemauan, dan tingkah laku sehingga fungsi fisik, sosial, ekonomi, dan pekerjaan terabaikan karna ketidak mampuan menilai kenyataan

Aplication of Mental Nursing Care on Mrs. P with Perceptual Sensory Disorders: Auditory Hallucinations

Halusinasi benar-benar nyata dirasakan oleh klien yang mengalaminya, sepertimimpi saat tidur. Klien mungkin tidak punya cara untuk menentukan persepsitersebut nyata, sama halnya seseorang seperti seseorang yang mendengarkansiaran ramalan cuaca dan tidak lagi meragukan orang yang berbicara tentangcuaca tersebut. Ketidakmampuan untuk mempersepsikan stimulus secara realdapat menyulitkan kehidupan klien. Karenanya halusinasi menjadi prioritasuntuk segera diatasi

Gene Therapy to the Retina and the Cochlea

Vision and hearing disorders comprise the most common sensory disorders found in people. Many forms of vision and hearing loss are inherited and current treatments only provide patients with temporary or partial relief. As a result, developing genetic therapies for any of the several hundred known causative genes underlying inherited retinal and cochlear disorders has been of great interest. Recent exciting advances in gene therapy have shown promise for the clinical treatment of inherited retinal diseases, and while clinical gene therapies for cochlear disease are not yet available, research in the last several years has resulted in significant advancement in preclinical development for gene delivery to the cochlea. Furthermore, the development of somatic targeted genome editing using CRISPR/Cas9 has brought new possibilities for the treatment of dominant or gain-of-function disease. Here we discuss the current state of gene therapy for inherited diseases of the retina and cochlea with an eye toward areas that still need additional development.

Sensitive Skins May Be Neuropathic Disorders: Lessons from Studies on Skin and Other Organs

Sensitive skin can be considered a neuropathic disorder. Sensory disorders and the decrease in intra-epidermal nerve ending density are strong arguments for small-fiber neuropathies. Sensitive skin is frequently associated with irritable bowel syndrome or sensitive eyes, which are also considered neuropathic disorders. Consequently, in vitro co-cultures of skin and neurons are adequate models for sensitive skin.

Spatial transcriptomics reveals unique molecular fingerprints of human nociceptors

Single-cell transcriptomics on mouse nociceptors has transformed our understanding of pain mechanisms. Equivalent information from human nociceptors is lacking. We used spatial transcriptomics to molecularly characterize transcriptomes of single dorsal root ganglion (DRG) neurons from 8 organ donors. We identified 10 clusters of human sensory neurons, 6 of which are C nociceptors, 1 Aβ nociceptor, 1 Aδ, and 2 Aβ subtypes. These neuron subtypes have distinct expression profiles from rodents and non-human primates and we identify new markers for each of these subtypes that can be applied broadly in human studies. We also identify sex differences, including a marked increase in CALCA expression in female putative itch nociceptors. Our data open the door to new pain targets and unparalleled molecular characterization of clinical sensory disorders.One Sentence SummaryThree A-fiber mechanoreceptor and seven nociceptor subtypes are identified, revealing sex differences and unique aspects of human DRG neurons.

Innocuous pressure sensation requires A-type afferents but not functional ΡΙΕΖΟ2 channels in humans

The sensation of pressure allows us to feel sustained compression and body strain. While our understanding of cutaneous touch has grown significantly in recent years, how deep tissue sensations are detected remains less clear. Here, we use quantitative sensory evaluations of patients with rare sensory disorders, as well as nerve blocks in typical individuals, to probe the neural and genetic mechanisms for detecting non-painful pressure. We show that the ability to perceive innocuous pressures is lost when myelinated fiber function is experimentally blocked in healthy volunteers and that two patients lacking Aβ fibers are strikingly unable to feel innocuous pressures at all. We find that seven individuals with inherited mutations in the mechanoreceptor PIEZO2 gene, who have major deficits in touch and proprioception, are nearly as good at sensing pressure as healthy control subjects. Together, these data support a role for Aβ afferents in pressure sensation and suggest the existence of an unknown molecular pathway for its detection.