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Hello, apologies. Everyone. There was some technical issues. Sorry, can I be heard now? Can everyone hear me? Wonderful apologies about that? I thought I've gone live but I haven't apparently so. I'm just gonna start from the beginning. Um My name is Lyn. Uh and I'm one of the academic clinical fellows in Neurology and a current to I MT three and soon to become a neurology registrar at Sheffield teaching hospitals. And today we'll be discussing uh cognitive and behavioral disorders, dementias and we're gonna dive a bit into auditory and visual cognitive impairments. And what I want you to get out of this session is basically be able to assess someone that comes to you with cognitive impairment or delirium and know exactly what work up you need to do in order for you to be able to direct further management and no um the evidence based workup and the evidence based management and then understand that course of the disease to be able to appreciate the prognosis and how to deliver that to patient and what can we do to help these patients? So, starting with uh the definition of dementia, it's basically a complex process and it involves uh quite a complex interplay between molecular pathways that affect the cellular functions in the brain. And therefore, this could lead to loss of synaptic connections, cell death, gliosis, inflammation and disruption of functional networks that underlie the cognition and the personality, as well as the behavior and sensory motor functions. And eventually that uh that starts attacking the individual's autonomy when all these domains become affected and aging by itself is the most robust risk factor for dementia. With more than 90% of dementias they present after the age of 65 years old. And according to a 2015 World Alzheimer's report, which is a comprehensive meta analysis. It estimated that at least now 46 million people worldwide are living with dementia, but they expect that number to almost triple by 2050 to at least 1 31 million. So as we can see, this is something that's now becoming more uh common because we have a more aging population, but it has its own implications on the patient's life. The patient's wellbeing, the patient's quality of life and their carers, quality of life. So, understanding uh the cognitive impairment and dementia better will help us uh be able to help these patients live with a relatively good quality of life for uh as much as possibly uh we can. And I'm going to also go through some of the risk factors that could potentially be contributing to this, that we could try to prevent early on. Um historically, the definitions of dementia have been weighed mainly towards memory and that's what we usually see in typical amnestic Alzheimer's disease. But that was revised in 2011 and started to reflect the plethora of cognitive and behavioral changes that caused the decline from the baseline levels of functioning. Now, the revised definition requires impairment in at least two neuropsychiatric or cognitive domains that we cannot explain by a nondegenerative or primary psychiatric disorder or a systemic condition such as delirium. Now, the diagnostic process is therefore, so, so requires us to have a very thorough history from the patient and uh preferably also a reliable informant as well as an objective measurement of that impairment. And we have specific neuropsychiatric and neuropsychological assessment tools that helps us objectively uh assess the degree of impairment in each patient. And um having a look at all patients who present with dementia as most of it has either a degenerative or a vascular cause. But there are other causes that we see such as infection, inflammation, neoplasms, toxic insults, metabolic disorders and trauma. And actually 11 to 14% of dementias are potentially caused by reversible conditions. And therefore, we need to rule out these conditions. It's very important because before we label the patient as dementia, if there are things that we can reverse to prevent any deterioration, we should uh now what I want you to know from this this has too many details in relation to the genetic basis of some of these neurodegenerative conditions causing dementia. But this is something uh this is just to show you different pathologies that cause different presentations. Um with amyloid beta, for example, um pri proteins, um alpha cy nuclein and Lewy bodies tau, all of these are misfolded proteins that accumulate at a very high um degree in the brain. And this is what causes the neurodegenerative process to go. And there are many ge genes that has been implicated in different uh neurodegenerative conditions. Um None of which you need to know about in detail. But obviously, anyone who has a strong family history of early onset dementia, we then need to consider checking these genes to see whether there is any connection to that. Because obviously, that has an implication on the wider uh family and conception and so on and so forth. But the most uh commonly known causes of neurodegeneration that causes dementia is uh prion disease or Cruce Jacob disease. And there are more than one type of crus Jacob disease. Uh There is fatal familial insomnia, Justman Toler, uh Schenker syndrome, and then Alzheimer's disease and Alzheimer by itself can have many subtypes like an AMN lit onset, a behavioral dis dis executive, uh Alzheimer's loic variants and a posterior cortical atrophy variant. And then we have the uh frontotemporal dementia, which uh as you all may know, we have a behavioral and a nonfluent variant of it. There is a semantic variant. There is one that overlaps with the presentation of M and D. There's corticobasal syndrome and then there's progressive supranuclear ballsy syndrome. And then lastly, the Lewy body dementia and Parkinson's disease dementia. Um So as I discussed um earlier in the uh earlier slides, the log can span quite a lot of things. And when we are taking history and do a physical examination, we need to try to narrow these down to know what to investigate for. So we know what to label the patient because that can, that can help us provide the best treatment for them. So, obviously, vascular causes like small vessel disease or history of strokes in the past could potentially increase the risk of developing cognitive impairments and dementia. If there is any neoplasm that would cause more likelihood for patients to present with cognitive impairment, uh psychiatric uh causes, for example, anxiety and depression. If it's longstanding and not very well treated, we actually see patients that present with um what we call a pseudodementia. So that because of the depression, um that hasn't responded to medications or has been going for a very long time, they will present with what looks like um cognitive impairment. When in fact, it's uh and that's why it's labeled pseudodementia, but they actually don't have any organic causes for the cognitive impairment they're struggling with. It's mainly related to ongoing s and longstanding depression, neurological So things like uh normal pressure, hydrocephalus is something that could cause quite a significant cognitive impairment and is reversible. So, it's important to rule out uh any toxins like toxic uh long term exposure to toxins like lead and mercury could potentially lead to build up and causing cognitive impairment. Uh and that, that used to happen more often in the past um inflammation. So, um diseases like multiple sclerosis, um and inflammatory uh conditions generally in the brain tend to put the patients at a higher risk of developing cognitive impairment infections. So, different types of types of encephalopathy or encephalitis, like anti NMDA encephalitis, uh herpes encephalitis, all these could potentially cause long term cognitive impairment. Uh traumatic brain injury is one of the leading causes of cognitive impairment. Um and uh people who have traumatic brain injury on the long term are put at a high risk of developing that. And then any endocrinological meta metabolical and nutritional deficiencies could present that way. So b12 deficiency folate deficiency, uh sometimes your um electrolyte imbalances by themselves could potentially cause that. So we need to be thorough when we are assessing uh as well as working of these patients before we label it with a specific subtype. Um So for us to be able to assess this, we need to have uh an understanding of the urgent considerations in this um aspect. Uh So we need to understand what delirium is and it's usually an acute reversible metabolically induced state of fluctuating consciousness. And it involves rapid changes in the level of consciousness and in the orientation. And usually if we have any signs, uh.