Неврологические расстройства

Introduction: Restless Leg Syndrome (RLS) is a known phenomenon observed in individuals experiencing opioid withdrawal, which can worsen heroin dependence. Typically,RLS affects only the legs, but this case report presents a unique instance of generalized Restless Body Syndrome (RBS) induced by opioid withdrawal.
Case presentation: The report describes a 67-year-old male undergoing opioid detoxification who experienced restlessness throughout his body, resembling RLS sensations.The restlessness affected various areas, including the thorax, abdomen, back of legs, lower back, arms, and legs, excluding the face. The sensations were described as periodic electric waves that intensified at night or during periods of inactivity and improved with physical activity, mainly walking. Similar sensations were also noted during withdrawal from opioids or buprenorphine/naloxone, significantly when the dose was reduced to 1mg/day, and they resolved upon reintroduction of buprenorphine/naloxone.
Results: Neurological examination revealed specific abnormalities, such as recent impaired recall, facial akinesia, decreased blink frequency, cog wheeling in upper extremities,a stooped, shuffling gait, and resting tremor in both upper extremities. Neuropsychiatric tests showed abnormal results in the Go-No-Go Test (4/6) and a minimal level of depression according to the Beck Depression Inventory Type-II (score: 9). The patient also scored as a problem drinker on the Michigan Alcohol Screening Test (score: 35).
Discussion: Exploration of the similarities between RBS and RLS, highlighting that RBS affects additional areas of the body, including the upper extremities, thorax, and back. While RBS may represent a variant of RLS, it could also be a different condition. Another potential explanation is that it may be a form of serotonin syndrome induced by opioid use, including fentanyl, which can lead to generalized myoclonus. Although RLS associated with opioid withdrawal is well-documented, the underlying mechanisms responsible for its manifestation throughout the body, including the neck, remain unclear. One hypothesis suggests a generalized polyneuropathy affecting the upper limbs and lower extremities, particularly in cases of iron deficiency. The report suggests that variants of RBS may occur in individuals undergoing opioid withdrawal, potentially requiring low-dose opioids for treatment. Consequently, evaluating RBS as part of the assessment for opioid withdrawal is necessary.

Introduction: Acute Necrotizing Encephalopathy (ANE) is a rare severe disease with high mortality or severe neurological sequelae characterized by rapid onset of consciousness disturbance and symmetric bilateral thalamic necrosis shown on imaging. To date, there have been limited investigations on SARS-CoV-2-related ANE, mainly in the form of case reports.
Case presentation: A previously healthy 13-year-old girl presented with rapid deterioration of consciousness, status epilepticus, elevated aminotransferase, and symmetrical multi-focal brain lesions on MRI images during the Omicron pandemic. She accepted mechanical ventilation and had a good response to plasma exchange and continuous blood purification, intravenous immunoglobulin and high-dose methylprednisolone.
Conclusion: ANE is a rapidly progressing disease that necessitates prompt detection through a combination of clinical presentation and imaging modalities. It is of paramount importance to enhance the awareness and knowledge of pediatricians regarding SARS-CoV-2-related encephalopathy. Upon diagnosis, treatment with high-dose intravenous methylprednisolone and IVIG should be contemplated. Additionally, plasma exchange and continuous blood purification could help alleviate liver damage in patients with ANE.

Objective: Correlation of Bluetooth transmission with subjective hyperosmia.
Background: Subjective hyperosmia, as a manifestation of belief of exposure to Bluetooth transmission, with testing demonstrating the absence of true hyperosmia, has not heretofore been described.
Case presentation: This 53-year-old right-handed single woman presented with a 10-year history of increased sensitivity to the aroma and enhanced perception of smells upon exposure to Wi-Fi electromagnetic radiation. She noted an intensity-duration effect: With higher intensity and duration of Wi-Fi exposure, her sense of smell would escalate and persist: After a few hours of exposure, her smell would jump to 190% of normal and last for two weeks.
Result: Abnormalities in the neurological examination: Reflexes: 0 in both lower extremities. Chemosensory Testing: Alcohol Sniff Test: 8 (hyposmia). Gustation: Waterless Empirical Taste Test: Brothy: 4/8 (hypogeusia).
Discussion: Nidus for such hyperosmic delusions may be a primary olfactory system disorder, with induction of ephaptic transmissions, causing intermittent phantosmia or otherwise misperceived odor, misattributed to the ambient environment. The assignment of the source of the hyperosmia to Bluetooth is consistent with the zeitgeist of mistrust and paranoia of higher technology. This may be a form of expectation effect due to visual evidence (high tower wires); suggestion combined with subcultural group dynamics with belief in harm of such electromagnetic/Bluetooth waves, with distorted information recall and misattribution. Suchgroup dynamics and shared misperceptions may fuel a delusion, as in the Mandela effect. Perchance, this case represents not having delusional hyperosmia due to a functional psychiatric disorder but instead having a neuroanatomic basis. Those with subjective hyperosmia and hypersensitivity to aromas have demonstrated hypertrophied gray matter volume in the posterior sub-region of the right hippocampus, left precuneus, left superior frontal gyrus, and right hypothalamus. In those with subjective hyperosmia, a neurological investigation is warranted.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of extracellular amyloid-β peptides (Aβ) and intraneuronal neuro-fibribillary tangles in the brain. Increasing evidence builds a strong case for the role of soluble Aβ oligomers (AβOs) in the impairment of insulin signaling in AD. Insulin signaling pathway begins upstream at the insulin receptor by phosphorylating IRS1 and propagating the signal downstream to the PI3K/ Akt which down-regulates GSK3β activity for tau phosphorylation and activates mTORC1 that mediates a wide range of cellular functions. Our study found that human AD brains had high levels of Aβ peptides with cerebral amyloid angiopathy (AD/CAA) and showed low activities of insulin signaling-responsive transcription factors as compared to age-matched non-demented controls (ND). Our further studies with neuroblastoma 2a (N2a) cells stably transfected with a human AβPP695 gene (N2a-AβPP), which secrete excessive Aβ, show that the basal levels of the expression and phosphorylation of several but not all critical signaling proteins along insulin signaling pathway are dysregulated as compared to the parental N2a cells. N2a-AβPP cells were phenotypically insulin resistant in response to insulin stimulation. Pre-treatment of N2a-AβPP cells with the Aβ-binding peptide (ABP), which binds and removes Aβ oligomers, significantly enhanced insulin signaling response in cells compared to controls. Taken together, our data suggest that human AD/CAA brains had dysregulation of insulin signaling and that Aβ oligomers may be responsible for inducing the insulin-resistant phenotype in N2a-AβPP cells and the removal of Aβ oligomers by ABP improved insulin signaling and relieved insulin resistant phenotype.

Context: The presence of anxiety in individuals with Coronary Heart Disease (CHD) is widespread, and it is related to a higher risk of negative outcomes. There has been a dearth of research on the management of anxiety in people with coronary artery disease.

Aims: The present study aimed to determine the associated risk of anxiety among Coronary Artery Disease (CAD).

Settings and design: This was a cross-sectional study conducted on a group of patients with IHD between the ages of 20 and 60 years.

Methods and material: A total of 200 individuals participated. Medical records were one of the data sources. The data of patients who meet the selection criteria gathered from the cardiology departments of the PSCC in KFSH.

Statistical analysis used: Statistical package for Social Science (SPSS) version 23 was used for statistical analysis.

Results: This research comprised 200 patients, the majority of whom were male (81%) and female (19%). According to the findings, 70% of people had minimal depression, 13.5% had mild depression, 8.5% had moderate depression, 4.5% had severe depression, and 3.5% had moderately severe depression. Medications were utilized in the majority of cases (98%).

Conclusion: Anxiety disorders that manifest themselves in the setting of heart disease must be recognized and treated with caution in the early stages of the disease. When giving medical therapy, it is important to examine the effects of the drugs on the heart, as well as the possibility of drug-drug interactions.