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Objective: To highlight the inflammatory and immunological mechanisms involved in depression and psoriasis. Methods: A comprehensive literature search was performed in various databases, in total 145 studies were selected. Results: Depression and psoriasis have an association. Immune mechanisms -the actions of tumor necrosis factor-a, interleukin 1 (IL-1), IL-2, IL-10, IL-22, IL-17, interferon-7, IL-1ß, prostaglandin E2, C-reactive protein, IL-6, and IL-8 etc.-, and some genetic changes are involved. Conclusions: A possible bidirectional relationship of psoriasis and major depression exists; i.e. the depression leads to psoriasis, and psoriasis leads to depression. We recommend more studies in the future to get a deeper and better understanding about this relationship. RESUMEN Objetivo: Poner de relieve los mecanismos inflamatorios e inmunológicos involucrados en la depresión y la psoriasis. Métodos: Se realizó en varias bases de datos una búsqueda bibliográfica completa; en total se incluyeron 145 estudios. Resultados: Hay asociación entre depresión y psoriasis y están involucrados mecanismos inmunitarios -las acciones del factor de necrosis tumoral alfa, las interleucinas (IL) 1, 2, 10, 22 y 17, el interferón gamma, la IL-1ß, la prostaglandina E2, la proteína C reactiva, la IL-6 y la IL-8, etc. - y algunos cambios genéticos. Conclusiones: Hay una posible relación bidireccional entre psoriasis y depresión, es decir, la depresión lleva a psoriasis y la psoriasis lleva a depresión. Se recomiendan más estudios en el futuro para obtener una comprensión más profunda y mejor sobre esta relación.

Understanding social cognition has become a hallmark in deciphering autism spectrum disorder. Neurobiological theories are taking precedence in causation studies as researchers look to abnormalities in brain development as the cause of deficits in social behavior, cognitive processes, and language. Following their discovery in the 1990s, mirror neurons have become a dominant theory for that the mirror neuron system may play a critical role in the pathophysiology of various symptoms of autism. Over the decades, the theory has evolved from the suggestion of a broken mirror neuron system to impairments in mirror neuron circuitry. The mirror neuron system has not gained total support due to inconsistent findings; a comprehensive analysis of the growing body of research could shed light on the benefits, or the disadvantage of continuing to study mirror neurons and their connection to autism.

A rare kind of antibody, known as anti-glutamic acid decarboxylase (GAD) autoantibody, is found in some patients. The antibody works against the GAD enzyme, which is essential in the formation of gamma aminobutyric acid (GABA), an inhibitory neurotransmitter found in the brain. Patients found with this antibody present with motor and cognitive problems due to low levels or lack of GABA, because in the absence or low levels of GABA patients exhibit motor and cognitive symptoms. The anti-GAD antibody is found in some neurological syndromes, including stiff-person syndrome, paraneoplastic stiff-person syndrome, Miller Fisher syndrome (MFS), limbic encephalopathy, cerebellar ataxia, eye movement disorders, and epilepsy. Previously, excluding MFS, these conditions were called ‘hyperexcitability disorders’. However, collectively, these syndromes should be known as “anti-GAD positive neurological syndromes.” An important limitation of this study is that the literature is lacking on the subject, and why patients with the above mentioned neurological problems present with different symptoms has not been studied in detail. Therefore, it is recommended that more research is conducted on this subject to obtain a better and deeper understanding of these anti-GAD antibody induced neurological syndromes.

Stiff-person syndrome (SPS) is a rare disorder that affects the central nervous system and is characterized by progressive muscle stiffness, rigidity, and spasm of axial and limb muscles. The syndrome is caused by a lack of gamma aminobutyric acid (GABA), which occurs because of antibodies against glutamic acid decarboxylase (GAD), an essential enzyme for GABA synthesis. Hence, the patients present with increased muscular activity. In this article, we will discuss two case studies of stiff-person syndrome.

Parkinson's disease is a widespread neurological illness. However, its psychiatric links have also been discussed lately by many authors, which has brought more depth to the specialized field of neuropsychiatry. Neuropsychiatric complications are commonly seen in Parkinson's patients, including major depression, anxiety, psychosis and hallucination, and cognitive abnormality. Almost all of these complications have a distinct pathophysiology and treatment. In this article we review the most recent studies about the association of these symptoms with Parkinson's disease and highlight the epidemiology, diagnosis, pathophysiology, and treatment of the neuropsychiatric complications, with more emphasis on the pathophysiology of these complications.

Little has been known about the possible brain changes in the patients suffering from the psychiatric illness called Dissociative Identity Disorder (DID). This review suggests that the patients of DID have structural changes in the limbic system–hippocampus and amygdala -and the cortex. Blood flow is also altered in the orbito-frontal cortex. Another interesting finding of this review is that the glutamate release is found to be the cause of the dissociative symptoms. Furthermore, this review also highlights that in some DID patients the dorsolateral prefrontal and parietal cortex are activated. The limbic system especially the amygdala and the dorsolateral prefrontal and parietal cortex are associated with the short term and working memory, while the hippocampus is associated with long-term memory. All of these regions are somehow affected in the DID patient’s brain. Thus, this explains the symptoms of the multiple personality changes and forgetting about the previous personality. However, the future studies will broaden our knowledge about the complete neuropsychiatry of this unique medical illness.

Objective: The aim of this paper was to highlight the mechanisms involved and the relationship between depression and psoriasis. Method: A comprehensive literature search was performed in various databases, and finally 88 studies were deemed relevant. Results: A significant link was found between depression and psoriasis, primarily through immune mechanisms related but not limited to the actions of inflammatory cytokines such as tumor necrosis factor-α, interleukin 1 (IL-1), IL-2, IL-10, interferon-γ, IL-1β, prostaglandin E2, C-reactive protein, IL-6, and IL-8. Conclusion: Various neuroimmunological studies point towards the notion that depression and psoriasis are associated with each other. Melatonin has also been found to be associated with both conditions. A possibility exists that both conditions can cause each other due to the possible bidirectional relationship of psoriasis and major depression. However, if this is the case, then why all depressed patients fail to develop psoriasis and why all psoriatic patients fail to develop depression remains a question unanswered. We believe that future studies will unmask this mystery.

The dearth of child psychiatrists in Pakistan is becoming one of the major causes of many cases of attention deficit hyperactivity disorder (ADHD) remain undiagnosed. Some important measures must be taken at the private and the governmental levels, so that the ADHD cases do not remain diagnosed in the future.

A literature search was conducted in different databases to study the topic of liver problems and diabetes. The aim of the study was to explore more about an association of diabetes mellitus with the liver. The study shows that diabetes does indeed have an effect on liver. Similarly, liver problems like chronic liver disease lead to diabetes which is known as hepatogenous diabetes. Common liver problems seen in diabetes patients include but not limited to fatty liver, decreased glycogen levels, risk of liver cancer etc. Like any medical problem, any knowledge about any subject is never enough, therefore we recommend more studies in the near future to broaden our understanding about the association of the liver with diabetes.

In this article, we discussed a clinical problem known as cardio renal syndrome (CRS). In CRS, both, the affected cardiovascular system, either low output or high output failure leads to the renal dysfunction or vice versa. As already known, the heart failure is the leading cause of readmission in the US and worldwide. The patients suffering with cardiac failure need extra care, as they may develop various complications. Cardiac output is affected in heart failure and does have an impact on the renal function. High cardiac output and low cardiac output, both can lead to renal dysfunction. In conclusion, we will also highlight some information about the prevention of the renal damage associated with the CVS. However, future research is recommended to understand more about the exact pathophysiology involved in this association.

We present a rare case of visual release hallucinations also referred to as Charles bonnet syndrome. The disorder is rare and no officially recognized mode of treatment has been developed. However, we hope that as the time goes by, and more cases of CBS are found. It will be possible for the scientists and the clinicians to find a permanent and a better cure for this rare mystery.

A large number of patients do not have cauda equina syndrome (CES) on MRI to account for their clinical findings; consequently, the majority of urgent scans requested are normal. We aimed to determine whether any clinical manifestation of CES, as stated in Royal College of Radiology guidelines, could predict the presence of established CES on MRI. We also aimed to support a larger study to develop a more universal assessment tool for acute lower back pain. A retrospective analysis of consecutive patients who warranted urgent MRI was conducted. Seventy-nine patients were eligible for study. The Kendall’s tau test was used for statistical analysis of all data. A p value of less than 0.05 was considered to be significant. MRI was performed in 62 patients out of 79. A total of 32.9% of patients had scans within 24 hours of admission. Nine of these patients were referred to neurosurgery for urgent neurosurgical review. Of these, 6.3% of patients had an established CES on MRI scan. One patient who had an out-patient MRI spine (15 days from hospital presentation) was found to have an established CES, was urgently referred to spinal surgery and underwent primary fenestration excision of the lumbar vertebra. No clinical features that were able to predict the presence of an established CES on MRI were elucidated. Findings included decreased anal tone 7.6% ( p = 0.282), faecal incontinence 3.8% ( p = 0.648), urinary retention 7.6% ( p = 0.510), bladder incontinence 8.9% ( p = 0.474), constipation 2.5% ( p = 0.011) and saddle anaesthesia 8.9% ( p = 0.368). Patients who had an abnormal MRI spine for back pain prior to this presentation showed a correlation with a newly diagnosed CES on MRI ( p = 0.016) with a correlation coefficient of 0.272.