There are three major groups of seizures:

Generalised Onset Seizures -

These seizures affect both sides of the brain or groups of cells on both sides of the brain at the same time. This term was used before and still includes seizure types like generalised tonic-clonic, absence, or atonic to name a few. 

Focal Onset Seizures -

The term focal is used instead of partial to be more accurate when talking about where seizures begin. Focal seizures can start in one area or group of cells in one side of the brain.

• Focal onset aware seizures: When a person is awake and aware during a seizure, it’s called a focal aware seizure. This used to be called a simple partial seizure.

• Focal onset impaired awareness: When a person is confused or their awareness is affected in some way during a focal seizure, it’s called a focal impaired awareness seizure. This used to be called a complex partial seizure.

• A focal seizure can also spread to both sides of the brain and become tonic-clonic (focal to bilateral tonic-clonic). People with this seizure type usually have an aura before the tonic-clonic seizure. 

Unknown Onset Seizures -

When the beginning of a seizure is not known, it’s now called an unknown onset seizure. A seizure could also be called an unknown onset if it’s not witnessed or seen by anyone, for example when seizures happen at night or in a person who lives alone. 

• There are two major classes or groups of seizures: focal onset and generalized onset.

• Focal onset seizures start in one area and can spread across the brain and cause mild or severe symptoms, depending on how the electrical discharges spread.

• Generalized seizures can start as focal seizures that spread to both sides of the brain. They also can occur as “generalized onset” seizures in which seizure activity starts simultaneously over both sides of the brain. Generalized onset seizures usually start during childhood and are similar to a thermostat surge or a light flash — abnormal regulation between parts of the brain causes the seizures.

2) How do neurological abnormalities contribute to the development of epilepsy?

• Problems in the brain's wiring, an imbalance of nerve signaling in the brain wherein some cells are unusually active or stop other brain cells from sending messages, or a few combination of these factors may develop epilepsy. EDIT

• Impaired regulation of the activation and resolution of inflammatory cells and molecules in the injured neuronal tissue is a critical factor to the development of epilepsy. Nonetheless, it is still unclear as to how the imbalance regulation of inflammation contributes to epilepsy. EDIT

  
  

3) What are the challenges in diagnosing epilepsy, particularly in distinguishing it from other neurological conditions?

It can be hard to diagnose epilepsy quickly as epilepsy is associated with difficulty and communicating can be seen as learning disabilities. Physical symptoms such as fainting, migraines and panic attacks are like other diseases and it can't be confidently picked up on without diagnosis unless there is more than 1 seizure.

4) How do anti-epileptic drugs work to control seizures, and what are the potential side effects?

Deep brain stimulation is a new treatment for epilepsy. The device records a patient's brain signals from the thalamus, which is used to help adjust the device by determining how often to send the pulses. Bursts of electricity sent along the wires can help prevent seizures by changing the electrical signals in the brain. DBS is a new procedure that's not used very often, so it's not yet clear how effective it is for epilepsy. 
 

Damaging the spinal cord which is connected to the nerves throughout the body creates a disconnection between the nerves in the lower body and the spinal cord. This is the least cause of paraplegia . 

There are rehabilitations techniques that are used such as yoga, water aerobics, weightlifting and seated aerobics 

to compensate the paralysis, professionals had created a Re-walk personal exoskeleton that provides powered hip and knee motion to allow individuals to assist in mobility.

Relationships change when people get spinal cord injuries. As finances change and the person deals with how to do their everyday life in a new way. As well as learning new coping methods as it affects mental health not being able to do thing as they used to. 

• MNDs can be distinguished from other neurological disorders by the pattern of motor and/or sensory involvement. MND can be inherited or sporatic. 

2. How do different types of MND vary in terms of symptoms and progression? 

• The different types of MND are determined by what parts of the body are affected, and how quickly the disease progresses. Each type is not a completely different disease, but a different form. You may be diagnosed with a type of MND based on how your symptoms originally present 

3. What are the potential genetic and environmental risk factors for developing MND? 

• The potential genetic and environmental risk factors include exposure to environmental toxins and chemicals, infection by viral agents, immune-mediated damage, premature aging of motor neurons, loss of growth factors required to maintain motor neuron survival and genetic susceptibility. 

4. What treatment options are available for MND, and how do they aim to manage symptoms? 

• Physiotherapy can help MND. In some cases, a medication called quinine can help treat muscle cramps too. They often improve later in the condition. 

5. What breakthroughs in research are being made to better understand the causes and potential cures for MND? 

• There’s currently no cure for MND. But research is bringing hope for the future. Countdown to a cure showcases how research has given us a much better understanding of MND, is pointing towards new ways to treat the condition and is taking laboratory discoveries nearer to the development of treatments. This means there are more potential treatments on the horizon and being tested in clinical trials than ever before. 

• Association funding has been crucial to Project AMBRoSIA, which has built one of the world’s largest collections of samples from people with MND. This resource has facilitated research which led to the discovery of a biomarker for MND – neurofilament light chain (NfL) – that measures motor neurone damage. This can now be used in clinical trials to help determine if a drug is working.   

• An innovative approach now allows more potential treatments to be tested in a clinical trial at the same time. Known as platform trials, this approach means more people with MND have the opportunity to take part and have a higher chance of receiving the treatment instead of placebo. Association funding is supporting the growth of these platform trials.   

1. What are the early symptoms of Alzheimer’s disease and how do they progress over time?

   • early symptoms of Alzheimer's disease can be as simple as misplacing an item, having trouble thinking of a word you want to use, having poor judgement and becoming more hesitant to try new things

   • symptoms can also be as big as repeatedly asking the same question, forgetting a recent conversation, forgetting the name of an object or person, mood changes and anxiety.

   • over time, these symptoms progress into serious memory problems and the loss to perform everyday tasks such as being able to communicate or having no awareness of the space you're in.

2. How do amyloid plaques and tau tangles in the brain contribute to the development of Alzheimer's disease?

• It is widely thought that these amyloid plaques contribute to the death of neurons in people with Alzheimer’s, either directly, or by causing another protein, called tau, to form toxic “neurofibrillary” tangles.

  3. what role do genetic factors like the APOE gene, play in the risk of developing Alzheimer's disease?

     • having two copies of APOE is associated with a higher risk of developing Alzheimer's than having one coping.

4. What are the current treatment options for the disease, and how effective are they in slowing the disease’s progression?

   • Although there are currently no forms of treatment that prevent Alzheimer’s disease completely, there are medications that are able to improve the severity of symptoms whilst preventing the decline in bodily functions. Two of these medications include:

   • Cholinesterase inhibitors. These medicines work by boosting levels of cell-to-cell communication. The medicines preserve a chemical messenger that is depleted in the brain by Alzheimer's disease. These are usually the first medicines tried, and most people see modest improvements in symptoms.

     Cholinesterase inhibitors may improve symptoms related to behaviour, such as agitation or depression. The medicines are taken orally or delivered through a patch on the skin. Commonly prescribed cholinesterase inhibitors include donepezil (Aricept, Adlarity), galantamine (Razadyne) and rivastigmine transdermal patch (Exelon).

     The main side effects of these drugs include diarrhoea, nausea, loss of appetite and sleep disturbances. In people with certain heart disorders, serious side effects may include an irregular heartbeat.

   • Memantine (Namenda). This medicine works in another brain cell communication network and slows the progression of symptoms with moderate to severe Alzheimer's disease. It's sometimes used in combination with a cholinesterase inhibitor. Relatively rare side effects include dizziness and confusion.

5. What promising research is being conducted to find a cure or more effective treatments for the disease?

   • Disease-modifying treatment strategies for Alzheimer disease (AD) are still under extensive research. Nowadays, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. Recent therapies have integrated multiple new features such as novel biomarkers, new neuropsychological outcomes, enrolment of earlier populations in the course of the disease, and innovative trial designs. In the near future different specific agents for every patient might be used in a “precision medicine” context, where aberrant biomarkers accompanied with a particular pattern of neuropsychological and neuroimaging findings could determine a specific treatment regimen within a customized therapeutic framework.

• In Multiple Sclerosis, the immune system becomes confused and attacks the protective myelin coating around nerves by mistake. If myelin is damaged, nerves can't communicate properly and may eventually die.

• Multiple Sclerosis  

  1. What strategies can help manage the effect of MS on cognitive functions? 

  Multiple sclerosis can affect one’s ability in significant ways, but there are strategies which could aid in the management of MS’s symptoms, including: 

  1. Cognitive Rehabilitation: Targeted cognitive training programs can improve memory, attention, processing speed, and problem-solving skills. 

  2. Compensatory Strategies: Use tools like calendars, reminders, and memory aids to compensate for cognitive challenges. 

  3. Fatigue Management: Prioritise rest, exercise regularly, and maintain a healthy sleep schedule to reduce fatigue's impact on cognition. 

  4. Stress Reduction: Engage in stress-reducing activities like meditation, yoga, or deep breathing exercises. 

  5. Physical Exercise: Regular exercise improves cognitive function, overall health, and mental well-being. 

  6. Cognitive Stimulation: Engage in mentally stimulating activities, such as reading, puzzles, or learning a new skill. 

  7. Medication Management: Adhere to prescribed medications and discuss any concerns with your healthcare provider. 

  8. Lifestyle Modifications: Maintain a healthy diet, limit alcohol consumption, and avoid smoking. 

   

   

  2. What recent advancements in MS research are showing promise for more effective treatments or a potential cure? 

  Briumvi (Ublituximab) is a prescription medication approved by the US FDA in 2022 for the treatment of relapsing forms of Multiple Sclerosis (MS), which includes: 

  Relapsing-Remitting MS (RRMS) 

  Active Secondary Progressive MS (SPMS) 

  Briumvi is a monoclonal antibody which targets CD20-positive B cells responsible for the contribution to MS’s symptoms and activity administered via intravenous infusion to reduce the frequency of relapses, delay progression and manage symptoms. The medication has beeen shown to reduce annualised relapse rates, decrease disability progression, and decrease the number of M2 lesions present on MRI scans. 

  3. How do psychological factors, such as stress and depression impact the progression and management of MS? 

  Stress can trigger or worsen MS symptoms, such as fatigue, pain, and cognitive difficulties. Depression can worsen symptoms such as fatigue, quality of life, and impact treatment adherence. 

1. Early signs of the disease include amnesia, mood swings, minor involuntary movements, clumsiness, trouble making decisions and trouble learning new things. Over time, these symptoms heighten in severity, small involuntary movements become jerky movements known as ‘chorea’, and people with the disease may have difficulties with simple tasks such as speech, swallowing, and concentration (BetterHealth Channel, 2022). In terms of psychological impact, cognitive decline is one of the main factors of the disease and in some cases may be present before the onset of motor disturbances (Anitha. A, 2023). 

2. Talk about how genetic mutation in the HTT gene leads to huntington’s disease.  

3. Motor symptoms associated with Hungtington’s disease are chorea which is causes movements that can’t be controlled. The involuntary movement affects muscles of the body, specifically the arms, legs, face, and tongue. Cognitive abilities associated with the disease would be having trouble prioritizing, organizing, or focusing on tasks.   Huntington's disease - Symptoms and causes - Mayo Clinic

5. There are currently active programs using antisense oligonucleotides (ASOs), RNA interference, small-molecule splicing modulators, and zinc-finger protein transcription factor. Except for ASOs and RNA interference approaches, the remaining therapeutic strategies are at a preclinical stage of development. Ribonucleic acid (RNA) is a molecule present in most living organisms and viruses. It is made up of nucleotides, which are ribose sugars attached to nitrogenous bases and phosphate groups. The nitrogenous bases include adenine, guanine, uracil, and cytosine. An antisense oligonucleotide (ASO) is a short single-stranded deoxyribonucleotide complementary to the sense strand of a selected nucleic acid. As a result, an ASO can modulate gene expression through several mechanisms. 

6. In the context of predictive testing for HD (Huntington’s disease), the questions are whether it is ethical to provide individuals with information about their future health when no treatment for the condition is available, what the beneficence, non-maleficence and justice issues are, and if the service is offered, how it should be conducted.