Insomnia can be defined as difficulty falling asleep or maintaining sleep, waking up earlier than expected, or having non-restorative sleep. It is one of the most common sleep disorders in the world. Insomnia is a common symptom of many neurodegenerative diseases but only recently has it been found that it is a risk factor for neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease.We did a traditional review to analyze the relationship between insomnia and neurodegenerative diseases. We analyzed all the relevant articles on Pubmed and included studies done on humans over the last 10 years with full text available.After reviewing the available literature on Pubmed, we conclude that insomnia is an important risk factor for neurodegenerative diseases. In addition, insomnia and neurodegenerative disorders have a complex and bi-directional relationship.We think it requires further study to understand the sole contribution of insomnia to the development of various neurodegenerative diseases when different factors like mood problems, genetic factors, and environmental factors also contribute to the disease. It would also be advisable to use cognitive screening questionnaires in all sleep clinics in insomnia patients over 50 years of age to diagnose dementia early and to gather more sleep study data for prospective and retrospective research. The role of hypnotics in preventing neurodegenerative diseases through treating insomnia should also be assessed.

Over the last decades several studies among the adult population have attempted to establish a correlation between the risk of stroke incidence and serum uric acid (SUA) concentration, and how these levels influence the patient's neurological outcome after a stroke. But, to date, the results are conflicting. In this review, an extensive literature search was performed through PubMed for articles published until May 2019 to review the association. The study selection was narrowed by searching PubMed database using the Medical Subject Headings (MesH) and associated keywords. Only articles conducted in English and on human subjects were included. We considered an article for this review if it had statistics on either the incidence, stroke mortality or post-stroke functional outcomes along with serum uric acid levels in adults. This review includes 21 articles with data of 33,580 cases of stroke and 1,100,888 participants. We can divide the articles reviewed into two separate cohorts of studies. One relates serum uric acid levels to stroke frequency and mortality, while the other is associated with serum uric acid and outcomes for stroke survivors. Based on our review, no significant relationship is observed with uric acid exhibiting protective effects on stroke outcome. Large clinical trials are advised to provide well-defined solutions to further assess the benefits of uric acid level lowering treatment in patients of vascular events, such as a stroke. However, we confidently report that increasing uric acid levels poses a higher risk for incidence of stroke.

Catatonia is a condition in which patients manifest with a complex of symptoms of behavioral and motor abnormalities. This condition can present with schizophrenia, bipolar, depression, and certain neurological illnesses. In this article, we analyze the coincidence of deep venous thrombosis (DVT) in schizophrenia with catatonia patients managed with electroconvulsive therapy (ECT) and the possible outcome of complications as an adverse event. The conclusion drawn from this traditional review reveals the importance of early diagnosis and treatment intervention of catatonia patients with ECT. No bleedingrelated complications occurred with the use of anticoagulants by catatonic patients managed with ECT and having underlying thrombosis. Literature also indicates that ECT can be safely administered for patients with distal deep venous thrombosis (DVT) treated with anticoagulants, while those with proximal DVT, ECT should be halted and anticoagulation treatment should be continued until the resolution of DVT to safely resume the ECT sessions. A possible alternative to ECT therapy for the patients with refractory schizophrenia with catatonia (who have safety concerns) is recombinant transcranial magnetic stimulation (rTMS). Nonetheless, more studies are needed to support our assertion.

Peripartum cardiomyopathy (PPCM) is a diagnosis of exclusion and a heterogeneous disorder that presents during the last month of pregnancy or the first five months postpartum. It is a rare but potentially life-threatening illness. A lot of work has been done trying to discover the causes of this condition, and several risk factors have been identified, including hypertension during pregnancy (HDP), ethnicity, advanced age, and multiple gestations. HDP affects 40% of cases of PPCM, and the strength of the association increases with increasing severity of hypertension. Among PPCM patients, there is a 1.5 times higher prevalence of HDP and a four-fold higher prevalence of preeclampsia (PE). Besides, the risk of PPCM markedly increases among women with HDP (5-21 times) compared with normotensive women. The experimental work done in animal models has provided support for the angiogenic-imbalance theory proposed regarding the association between these two conditions. The presence of the same risk factors also supports the prevalence of the coexistence of PE and PPCM. During the last part of gestation, the placenta secretes more anti-angiogenic factors, which leads to the development of both PE and PPCM. However, not all patients with HDP develop PPCM. In fact, most PPCM patients do not show any signs of HDP. Further work in these patients elucidated that there is an underlying susceptibility in some women that predisposes them to develop this condition and results in a worse prognosis as compared with those PPCM patients who have HDP. Better provision of care, genetic variations, and association with HDP have been cited as some of the factors affecting prognosis. HDP has also been found to increase the risk of other forms of cardiomyopathies in the future. A lot of work still needs to be done to uncover all the pathologic mechanisms and genetic variations involved in this disorder. More intensive and focussed research may help in developing new therapies to better manage this condition and address all of its complications.