Epilepsy is a complex disease with diverse clinical characteristics that preclude a singular mechanism. One way to gain insight into potential mechanisms is to reduce the features of epilepsy to its basic components: seizures, epileptogenesis, and the state of recurrent unprovoked seizures that defines epilepsy itself. A common way to explain seizures in a normal individual is that a disruption has occurred in the normal balance of excitation and inhibition. The fact that multiple mechanisms exist is not surprising given the varied ways the normal nervous system controls this balance. In contrast, understanding seizures in the brain of an individual with epilepsy is more difficult because seizures are typically superimposed on an altered nervous system. The different environment includes diverse changes, making mechanistic predictions a challenge. Understanding the mechanisms of seizures in an individual with epilepsy is also more complex than understanding the mechanisms of seizures in a normal individual because epilepsy is not necessarily a static condition but can continue to evolve over the lifespan. Using temporal lobe epilepsy as an example, it is clear that genes, developmental mechanisms, and neuronal plasticity play major roles in creating a state of underlying hyperexcitability. However, the critical control points for the emergence of chronic seizures in temporal lobe epilepsy, as well as their persistence, frequency, and severity, are questions that remain unresolved.

Guillain Barré syndrome is one of the best examples of a post infectious immune disease and offers insights into the mechanism of tissue damage in other more common autoimmune diseases. Controlled epidemiological studies have linked it to infection with Campylobacter jejuni in addition to other viruses including cytomegalovirus and Epstein Barr virus. The syndrome includes several pathological subtypes, of which the most common is a multifocal demyelinating disorder of the peripheral nerves in close association with macrophages. Evidence from histological examination of peripheral nerve biopsy and postmortem samples suggests that both cell mediated and humoral mechanisms are involved in the pathogenesis. Immunological studies suggest that at least one third of patients have antibodies against nerve gangliosides, which in some cases also react with constituents of the liposaccharide of C jejuni. In the Miller Fisher variant of the disease, these antiganglioside antibodies have been shown to produce neuromuscular block, and may in part explain the clinical signs of that disorder. Treatment with both intravenous immunoglobulin and plasma exchange reduces the time taken for recovery to occur, although mortality remains around 8%, with about 20% of patients remaining disabled.

People with Parkinson’s disease (PD) and their care partners frequently report cognitive decline as one of their greatest concerns. Mild cognitive impairment affects approximately 20–50% of people with PD, and longitudinal studies reveal dementia in up to 80% of PD. Through the Parkinson’s Disease Foundation Community Choice Research Award Program, the PD community identified maintaining cognitive function as one of their major unmet needs. In response, a working group of experts across multiple disciplines was organized to evaluate the unmet needs, current challenges, and future opportunities related to cognitive impairment in PD. Specific conference goals included defining the current state in the field and gaps regarding cognitive issues in PD from patient, care partner, and healthcare professional viewpoints; discussing non-pharmacological interventions to help maintain cognitive function; forming recommendations for what people with PD can do at all disease stages to maintain cognitive health; and proposing ideas for how healthcare professionals can approach cognitive changes in PD. This paper summarizes the discussions of the conference, first by addressing what is currently known about cognitive dysfunction in PD and discussing several non-pharmacological interventions that are often suggested to people with PD. Second, based on the conference discussions, we provide considerations for people with PD for maintaining cognitive health and for healthcare professionals and care partners when working with people with PD experiencing cognitive impairment. Furthermore, we highlight key issues and knowledge gaps that need to be addressed in order to advance research in cognition in PD and improve clinical care.

The co-occurrence of Borderline Personality Disorder (BPD) and Intellectual Disability (ID) is a sparsely covered area in the literature. This case series looks to describe the common presentations of these two disorders, both commonly presenting with self-harm, impulsivity, and intense anger. Additionally, three treatment courses of individuals with co-occurring ID and BPD will be described, illustrating the commonalities as well as the modifications of BPD treatment for individuals and in adapting ID supports for those with BPD. Of the 3,028 children, 16% of those without autism or a learning disability had been diagnosed with a psychotic disorder. And, for children who had autism or a learning disability, only 7% of those given antipsychotics had a psychotic disorder. Looking further at these records, we found that the children with an intellectual disability or autism were more likely to be given an antipsychotic drug. In fact, 2.8% of the children with an intellectual disability had been prescribed antipsychotics, and 75% of these had autism. By contrast, 0.15% of those without an intellectual disability had been prescribed the medication.

Multiple sclerosis (MS) is a chronic inflammatory autoimmune demyelinating disease of the central nervous system. It affects approximately 400,000 people in the United States and onset is usually during young adulthood. There are four clinical forms of MS, of which relapsing remitting type is the most common. As the etiology of MS is unknown, finding a cure will remain challenging. The main mechanism of injury appears to be inflammation and 8 agents are now FDA approved to help control MS. These agents for relapsing forms of MS target different parts of the immune system, with the end goal of decreasing and avoiding further inflammation. No agents are FDA approved for the primary progressive version of MS. FDA approved agents include four preparations of interferon ß (Avonex, Rebif, Betaseron and Extavia), glatiramer acetate (Copaxone), mitoxantrone (Novantrone), natalizumab (Tysabri) and fingolimod (Gilenya). There are several drug undergoing phase II and III trials. The heterogeneity of the MS disease process, individual patient response, and medication toxicities continue to challenge the treating physician.