Determination of plasma transcobalamin-II and zinc levels in newly-diagnosed and long-standing grand mal epileptic patients

Background: The changes of plasma transcobalamin-II (TCII) and Zinc (Zn) Levels in epileptic patients are not clearly understood. The aim of the current study was to evaluate the plasma contents of TCII and Zn levels in newly–diagnosed epileptic seizure patients, long-standing grand mal epileptic patients following treatment with sodium valproate and healthy control group. Methods: Thirty patients aged 36.76±12.91 years with newly–diagnosed and thirty long-standing grand mal epileptic patients aged 35.56 ±12.77 years were diagnosed based on the clinical symptoms. The control subjects were picked out from healthy individuals and matched to the patients, aged 36.30 ±12.80 years. Plasma Zn and TCN-2 was evaluated via spectrophotometry at 546 nm and 450 nm, respectively, using chimerical kits. Results: Plasma level of TCII in the newly–diagnosed epileptic seizures patients and long-standing grand mal epileptic patients were significantly increased, compared to the healthy controls 14.89 ±3.24 and 21.84± 2.73 vs. 9.55±1.24, (n=30), respectively. Plasma level of Zn was decreased in the newly–diagnosed epileptic seizure patients, while it was increased in long-standing grand mal epileptic patients compared to the control group 69.28± 6.41 and 80.56 ±6.12 and vs.75.80±1.59, (n=30), respectively. Conclusion: This study suggests that sodium valproate may disrupt the homeostatic balance of TCII and Zn, and cause abnormality of their serum level in newly–diagnosed epileptic seizure patients and long-standing grand mal epileptic patients. Further research is recommended to identify the underpinning for these changes. &#160

Astrocytic Abnormalities in Schizophrenia

Astrocytes are glial cells in the central nervous system (CNS), which contribute to CNS health and disease by participating in homeostatic, structural, and metabolic processes that play an essential role in facilitating synaptic transmission between neurons. Schizophrenia (SCZ) is a neuropsychiatric disorder associated with various positive and negative behaviors and interruption of executive function and cognition thought to be due partly to aberrations in signaling within neural networks. Recent research has demonstrated that astrocytes play a role in SCZ through various effects, including influencing immune system function, altering white matter, and mediating changes in neurotransmitters. Astrocytes are also known to play a role in inducing SCZ-associated changes in neuroplasticity, which includes alterations in synaptic strength and neurogenesis. Also, astrocyte abnormalities are linked to neurobehavioral impairments seen at the clinical level. The present chapter details general information on SCZ. It highlights the role of astrocytes in SCZ at molecular and behavioral levels, including neural changes seen in the disease, and the therapeutic implications of targeting astrocytes in SCZ

Lupus and the Nervous System: A Neuroimmunoloigcal Update on Pathogenesis and Management of Systemic Lupus Erythematosus with Focus on Neuropsychiatric SLE

An autoimmune condition is characterized by a misdirected immunological system that interacts with host antigens. Excess activation of T- and B-lymphocytes, autoantibody generation, immune complex deposition, and multi-organ injury are found in systemic lupus erythematosus (SLE), an early autoimmune condition with a substantial hereditary element. A number of environmental factors and lifestyle changes also play a role in the development of SLE. The imbalanced immunity could take part in the dysfunction and injury of different biological organs, including the central and peripheral nervous systems. Neuropsychiatric SLE (NPSLE) can present with focal and diffuse involvements. Clinical manifestations of NPSLE vary from mild cognitive deficits to changed mental status, psychosis, and seizure disorders. Headaches, mood, and cognitive problems are the most common neuropsychiatric presentations associated with SLE. NPSLE could be found in 40% of all people who have SLE. The diagnostic inference of NPSLE can be made solely following these secondary causes have been ruled out. The present chapter provides an updated discussion of the clinical presentation, molecular processes, diagnosis, management, and therapy of SLE with emphasizing on NPSLE

Surgical tool entrapment in a young patient with recurrent lumbar spinal stenosis: a case report

Key Clinical Message Lumbar spinal stenosis (LSS) is a prevalent cause of leg and back pain. In the youth, LSS is not common and mainly results from hereditary musculoskeletal disorders. Moreover, spinal fusion is a surgical approach to the treatment of LSS. Entrapment of surgical tools due to breakage is a rare yet important phenomenon in such operations. Therefore, neurological sequelae of these events need to be explored. The case was a 24‐year‐old male complaining of local back pain. Initially, he was diagnosed with LSS at L4 and L5. After the fusion of the vertebrae by the posterior spinal fusion (PSF) method, the patient's pain was resolved. However, the subject complained of worsening local back pain limiting his ability to do routine tasks. A few years later, radiographical evaluations indicated the possible presence of a surgical tool that could not be removed via surgery. During a third operation, the object was removed, and the patient's symptoms recovered. Immediate removal of entrapped surgical objects is necessary due to risks associated with migration and central nervous system damage. Comparing our results to other similar reports, we conclude that in cases of foreign object entrapment, neurological sequelae may be nonexistent or progressively worsen. Also, sequelae emerge either soon after the operation or emerge later. This complicates the diagnosis of such events and the decision of whether to subject the patient to additional neurosurgical operations to remove the tool. These variations may be observed due to the moving of the entrapped tool. Follow‐up of neurological sequelae in spinal surgery patients is recommended

Crocin attenuates the lipopolysaccharide-induced neuroinflammation via expression of AIM2 and NLRP1 inflammasome in an experimental model of Parkinson's disease

The underlying mechanisms of inflammasome activation and the following dopaminergic neuron loss caused by chronic neuroinflammation remain entirely unclear. Therefore, this study aimed to investigate the impact of crocin on the inflammasome complex within an experimental model of Parkinson's disease (PD) using male Wistar rats. PD was induced by the stereotaxic injection of lipopolysaccharide (LPS), and crocin was intraperitoneally administrated one week before the lesion, and then treatment continued for 21 days. Open field (OF) and elevated plus maze tests were applied for behavioral assays. Furthermore, hematoxylin and eosin (H&E) and immunostaining were performed on whole brain tissue, while dissected substantia nigra (SN) was used for immunoblotting and real-time PCR to evaluate compartments involved in PD. The time spent in the center of test was diminished in the LPS group, while treatment with 30 mg/kg of crocin significantly increased it. H&E staining showed a significant increase in cell infiltration at the site of LPS injection, which was ameliorated upon crocin treatment. Notably, crocin-treated animals showed a reduced number of caspase-1 and IL-1β positive cells, whereas the number of positive cells was increased in the LPS group (P < 0.05). A significant decrease in tyrosine hydroxylase (TH) expression was also found in the LPS group, while crocin treatment significantly elevated its expression. IL-1β, IL-18, NLRP1, and AIM2 genes expression significantly increased in the LPS group. On the other hand, treatment with 30 mg/kg of crocin significantly downregulated the expression levels of these genes along with NLRP1 (P < 0.05). In summary, our findings suggest that crocin reduces neuroinflammation in PD by diminishing IL-1β and caspase-1 levels, potentially by inhibiting the expression of AIM2 and NLRP1 genes

Deep brain stimulation (DBS) as a therapeutic approach in gait disorders: What does it bring to the table?

Gait deficits are found in various degenerative central nervous system conditions, and are particularly a hallmark of Parkinson’s disease (PD). While there is no cure for such neurodegenerative disorders, Levodopa is considered as the standard medication in PD patients. Often times, the therapy of severe PD consists of deep brain stimulation (DBS) of the subthalamic nucleus. Earlier research exploring the effect of gait have reported contradictory results or insufficient efficacy. A change in gait includes various parameters, such as step length, cadence, Double-stance phase duration which may be positively affected by DBS. DBS could also be effective in correcting the levodopa-induced postural sway abnormalities. Moreover, during normal walking, interaction among the subthalamic nucleus and cortex —essential regions which exert a role in locomotion— are coupled. However, during the freezing of gait, the activity is desynchronized. The mechanisms underlying DBS-induced neurobehavioral improvements in such scenarios requires further study. The present review discusses DBS in the context of gait, the benefits associated with DBS compared to standard pharmacotherapy options, and provides insights into future research