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Doctor Zo, I'm a neurologist, working as a stroke physician. At the moment in Kingsmill Hospital. I was asked to help you with the neurology uh questions. I was thinking about what would be the best way to present this talk. And I thought uh I'd like to do as real life presentation as possible. So, so I will give you a snapshot of a wide range of neurological conditions. And uh there is no form structure of this uh speech uh regarding topics. So it will be random topics, topics. One after the other, I'd like to start with an example of a uh uh for a neuropathy. A 60 year old man was referred to neurology with an isolated left hand weakness on examination. He has marked wasting in the dorsal inter muscles and limited movements in finger ebb and abduction. He had symmetrical normal, deep tendon reflexes and reduced sensation in digit four and five. What investigations would be the most useful in this case? Uh If we go through the the options, so chest X ray would be considered if you, if you suspect an epical lung uh cancer, uh the usual association is, is with Horner Syndrome. So, uh it was not indicated in this case, uh MRI brain and MRI C spine would be useful if you suspect any CNS pathology. But the examination findings all uh pointed to uh peripheral uh causes and the nerve conduction studies are more likely to show the expected finding which would be an ulnar nerve compression. As the patient had normal deep tendon reflexes and very limited sensation to the ulnar nerve territory. Brachial plexus pathology is less likely. This was an example of how important localization in neurology localization uh uh can be seen in different ways. Uh One common uh question when we see patients with motor uh presentations, whether the upper or the lower motor neuron is involved. Uh We all know whether that the muscle tone, deep tendon reflexes, the plantar reflexes. Uh uh Hoffman sign and muscle wasting can be variable uh present or or altered in the upper and lower motoneuron lesions. Uh This case showed a peripheral neuropathy where marked muscle wasting was part of the presentation. Uh muscle wasting is not uncommon in upper motoneuron lesions as well if there is chronic muscle wasting down to misuse atrophy. Next case is a 28 year old woman who saw the GP with a long history of fatigue, dizziness and imbalance. Her neurological examination showed normal cranial nerve function, normal upper limb and absent lower limb reflexes. She had diminished vibration sensation in her legs. She had an extensor plantar response and she had spinal ataxia with positive Romberg. What test would you recommend in the first place to try to identify a treatable medical problem based on the patient's uh neurological examination of you. You have to understand that the patient had some features of lower motor uh pathology because there was absent uh uh limb reflexes in the lower limbs. She had some sensory disturbance mainly affecting the posterior column and uh she also had uh upper motoneuron signs and the spinal ataxia in the Romberg's position. Uh the spinal ataxia, Romberg's usually uh means that the spinal cerebellar tract in the spinal cord is is involved. So, this combination of findings is all pointing to vitamin b12 deficiency or folate deficiency that manifests in pernicious anemia and uh subacute combined degeneration of the cord. So, this case was an example of a mixed upper and lower motoneuron features, upper motor neuron signs or features can be often seen in the CNS pathology. For example, people affected by a stroke, multiple sclerosis or traumatic brain injury, lower motor neuron signs can be expected to impure neuromuscular uh uh pathology such as polyneuropathy, muscular dystrophies, Guillain Barre syndrome or polymyositis. There are quite a few neurological disorders where upper and lower motor neurone features are mixed and can vary uh uh during the course of DNS. One example is motoneuron disease. Uh one of the cerebellar ataxia is called Friedrich ataxia has mixed, upper and lower motoneuron features more common disorders are vitamin beta deficiency or uh, degenerative cervical myelopathy. The next case, he is an elderly man with a long history of hypertension diabetes and recurrent strokes. He was brought to hospital with new onset swallowing difficulty. The wife told us that he has difficulty keeping his eyes open. In the evenings, he cannot finish a meal as he has increasing difficulty chewing and swallowing food. His voice is very weak at times. What do you think is the most likely cause of his swallowing trouble? Can it be a recent stroke? Can it be pseudo barber pai? Are there any features of motoneuron disease? Could this be myasthenia or temporal arthritis? The fluctuating nature of his uh uh swallowing difficulty and also uh the fluctuating ocular symptoms, the droopy eyelids that are make uh getting worse by the evening are all pointing to autoimmune myasthenia gravis, which often presents with fluctuating ocular and barbar weakness. This patient did not have headaches. So temporal arteritis would not be a question. In motoneuron disease, one would expect steadily progressive symptoms without any fluctuation and the brainstem stroke and pseudo pauses. Uh We should see other characteristic signs or symptoms. Another patient, um he's a nursing home resident with a history of recurrent strokes. Uh He was seen by the GP the carers were concerned about frequent episodes of crying, otherwise he's quite settled in the nursing home. He likes watching TV and playing with model trains. Uh on examination he had desire to speech and mind swallowing difficulty. What can be the most likely presentation or explanation of these of these symptoms? Could he have a recent stroke or does he suffer with senile depression? The episodic crying can be a symptom of epileptic seizures or pseudo barber po motoneuron disease could explain his speech and swallowing trouble. Most likely this patient has developed a pseudo barber palsy which is a condition when people develop progressive barber symptoms. And uh quite often emotional ability with sudden burst of crying and laughing, uh can be seen. Pseudobulb pa is due to a dysfunction of the corticobulbar fibers uh that connect uh the cortex uh to the lower brainstem dys osteo dysphagia and some signs of upper motoneuron pathology are commonly found. This can be a stiff tongue with limited tongue movements, brisk jaw jerk, enhanced g gag reflex. Uh pseudo barber posi usually represents diffuse brain involvement and the diffuser uh brain damage with cortical uh uh dysfunction often presents with emotional libid. Contrary to the pseudo psy patients, uh people who develop real bar palsy, uh have other signs that you can pick up on examination. One of them is the soft palate uh movements and tongue movements are limited down to uh neuromuscular weakness. Quite often we see a tongue wasting and uh fasciculations and the gag reflex, which is usually enhanced in a pseudo barber P is diminished. Palsy is often caused by bilateral dysfunction of the lower brainstem, uh uh motor nerves or myasthenia gravis. Next patient is a 46 year old man who is referred with chronic lower back pain and water sensation on the left lateral thigh. He told us that the skin on the left side is quite sensitive to touch and he often has painful pins and needles in the same area. He works as a zookeeper and he's very fit for his age. He can walk several miles without a problem but this painful sensation on the left side returns when he's standing for a long time or feeding the Rhinos, which test would be the most helpful. In this case, would MRI of the lumbar spine show anything? Uh could this be a problem with his hips, nerve conduction studies? Would it help anything? Uh would it help us to identify a peripheral nerve entrapment causing the symptoms because he has this uh sensation in the lower limb? Uh Could this be diabetes? I think the best answer is none of these. The patient describes uh meralgia polyesthetic, which is a condition where the lateral cutaneous nerve of the thigh is irritated by soft tissue stiffness or a scarring uh in the venal area. Quite often, this mechanical nerve irritation is caused by uh tight uh belts or tight clothes. And it is not uncommon in people who have recently lost or put on weight. The best management for these people is reassurance and their lifestyle advice when it comes to localization in neurology. Um A common clinical question is whether the ongoing symptoms are caused by central nervous system or peripheral nervous system pathology. There are cases where we can suspect central nervous system pathology by the by the symptoms, especially when people have cortical signs such as aphasia neglect, axia or a hemianopsia. There are also um cases mainly in the stroke, uh sufferers where people develop pure motor, pure sensory or sensory motor hemi symptoms or an atoxic hemiparesis. These are usually caused by lacunar strokes. People who suffer with spinal cord problems quite often have a sensory level, especially in acute spinal cord compression or transverse myelitis. So, detecting the sensory level, especially in the trunk is highly characteristic of a spinal cord pathology. Peripheral nervous system disorders. Co quite often present with a localized uh motor and sensory deficit. There are certain uh peripheral nerves that are more prone to mechanical irritation or uh or compressive uh damage. Um This case, these uh presentations can uh be common peroneal nerve pauses, radio nerve pauses, nerve entrapment, median nerve entrapment in carpal tunnel syndrome. And what I already mentioned, uh Meralgia Potica. Next question is about a 32 year old woman who went to the opticians with a history of severe morning headaches and blurry vision. She told the opticians that she couldn't see objects were in her peripheral vision. She had a visual fear test that showed bitemporal hemianopia, which test do you think would help us to reach a definite diagnosis. Is a lumbar puncture indicated in this case, should we send her to A&E for an urgent ct head? Or would it be better to have an MRI scan of the head as she has visual disturbance? Uh would an OCT help mainly to rule out retinal disease or early uh PPI edema. The morning headaches raise the possibility of obstructive sleep apnea. Would overnight pulse oximetry be indicated in this case. Uh The fact that this lady had bitemporal hemianopia on the visual fear testing is highly indicative of a compressive vision at the optic chiasm. The most likely cause is a pituitary macroadenoma in her age. And so I think an MRI scan of the head would be the most useful test visual field defect are not uncommon in uh uh neurological conditions. Uh Do you know this uh uh this figure and, and uh the different types of visual affi defects? I just like you to uh to be aware of uh conditions that uh come with monocular visual loss. People who develop visual fear defects, affecting both sides is uh highly suspicious of brain pathology so far. So, examples of uh the importance of localization in neurological disorders. The most people who present with neurological symptoms come with uh a combination of symptoms or some features that usually make the diagnosis. That's why neurologist used to say that uh history taking is the most important thing in neurology. The second most important thing is a neurological examination. So I think for the rest of the talk, uh we will go through a few uh or quite a few neurological conditions where, where history taking or the features probably make the diagnosis. This young man visited the GP with headaches. He often develops a headache at work, uh described as a symmetrical pressure headache across the frontal and parietal area. At times, it makes him feel a bit dizzy. Uh When the headache is bad, he likes to go out for a break. And the brisk walk or listening to music can uh make the headaches go away when he came to the doctor, the BP and the neuro exam was normal. What treatment would you recommend if the headaches get worse? Would propranolol topiramate be of any use for him? Paracetamol can be given to people with basically any type of headaches. Would a course of acupuncture be useful or would Botox carp injections be indicated? Uh So the description of this headache is more in keeping with the episodic tension headaches. If self management is not successful, people can try non steroid antiinflammatory drugs such as paracetamols, prop topiramate are used in a migraine prophylaxis. A course of acupuncture is uh is a recommended treatment by nice for people who have uh frequent or chronic tension headaches. Otoscopy injections are indicated in chronic migraine. So the most common headache disorders that people uh present with uh are tension headaches, migraine and uh cluster headaches. If you don't mind, I'd like to go through the main features of these headaches because they are so common that uh uh one in 10 people who visit GP is basically uh Oscar advisor on headache management. People who develop tension headaches usually have bilateral tightness, pressure sensation across the head. This headache is usually a a non pulsating headache and uh mild to moderate severity because this is usually am headache. It doesn't stop people doing uh their usual activities. There are not too many missed days from work. And uh and uh most people don't really see a GP with 10 headaches, duration of uh episodic tension headaches can be uh usually less than an hour to a few hours a day or some people develop chronic tension headaches, which can be basically an all day headache. Usually, uh don't stop them. Uh getting to sleep at night, there is very little activities and the headache is usually not aggravated by routine activities or, or sports activities. Other neurological symptoms are very rare in uh tension headaches. Although uh chronic neck pain or stiffness around the shoulders is not uncommon. Migraine is a more severe uh headache disorder compared to tension headaches. And uh most people who attend GPS uh for headache management suffer with migraine. The classic feature of a migraine attack is a unilateral pulsating headache of moderate to severe intensity. The headaches can last for a few hours up to a day or two during a migraine attack. Uh people have limited uh function as the headaches and the associated nausea. Dizziness can be aggravated by routine activities or any physical activity. Migraine is a complex uh chemical disorder of the brain. And uh one feature of migraine is increased sensitivity to light noise, strong smells, motion, migraine aura symptoms are also common. The classic uh migraine attack usually starts with an aura, usually visual disturbance or sensory symptoms, which is a spreading numbness or pins and needles starting on the face, spreading down to the upper limb or speech difficulty. Quite often uh manifesting as severe dysphasia can be present. These other symptoms are usually short lived uh neurological symptoms. They don't last more than 60 minutes. People who have prolonged oral symptoms and uh severe migraine headaches uh require brain imaging because uh it could be uh a symptom of underlying structure abnormalities such as an artery or venous malformation of brain tumors. The oral symptoms are sometimes can be mixed up with the seizure disorders. The nature of migraine aura that usually the symptoms are of gradual onset. And uh and uh there is a spreading uh feature in sensory symptoms compared to epileptic seizures when the symptoms start all of a sudden and uh the spreading uh of the symptoms are usually faster than in migraine can be measured more in seconds than in minutes. In what what we see in migraine. Another possible differential diagnosis to migraine oral symptoms is uh transient ischemic attacks, especially in the elderly population. So people who have ts usually the symptoms are suddenly short lived and the resolution of the symptoms is also quicker than in migraine. Another uh primary headache disorder is cluster headaches. Cluster headaches are quite often overdiagnosed because uh we quite we we see referrals from GPS that uh people have cluster headaches or cluster migraines. So the cluster uh word is quite often used in people who have a high frequency headaches, but cluster headaches is a distinct entity. And uh the positive features of the cluster headaches that are outlined here make the diagnosis and the and uh help us distinguish it from migraine or other types of headaches. Cluster headaches uh belong to a group of headache disorders called trigeminal autonomic cephalalgias, trine autonomic headaches are usually side locked headaches. So people have unilateral headaches quite often the headache, uh localization and the associated symptoms represent uh trigeminal nerve involvement. So the first division of the trigeminal nerve that supplies uh sensation to the periorbital area are usual is usually involved with cluster headaches. So that's why most people present with severe pain around or inside the eye socket. The pain quality is variable. It can be a pulsating, throbbing headache. But what is different from migraine and cluster headaches? That is a very severe one of the most severe types of pains. People can experience the duration of the cluster headache attacks, uh varies from 15 minutes to three hours. The behavior of people who have a cluster headache attack is quite different from people uh with tension or migraine headaches because quite often these people are pacing about you. They can't rest, they can't go to bed, they're quite agitated. There are other features that uh in my clinical practice I II can rely on. So for example, one feature is that it's very rare in women and more common in men, usually middle aged men who are heavy drinkers or uh heavy smokers. But certainly there are exceptions from this. This is just a general rule and uh alcohol, even small amount of echoes sometimes can bring on the headaches. There are other features of cluster headaches which are quite distinctive. These are mainly the autonomic symptoms. So the autonomic symptoms represent an activation of the parasympathetic system that originates from the hypothalamus. So during a cluster headache attack, quite often people have a droopy eyelid horners sy uh other features of Horners syndrome, increased uh uh secretions including la cremation, nasal congestion, uh erythema, sweating and swelling on the same side of the face. This patient uh went to the GP with uh daily severe headaches. She's a lady in her fifties. She has a long history of episodic migraines that were well managed with paracetamols and going to bed in a dark room. Over the last year, she developed a new type of headache. She has brief episodes with strictly right sided head pains around, mainly centralized around the eye socket. The pain is more severe than the post migraine and the right eyelid is quite often droopy during these attacks. In the past, she used to have migraines once every couple of weeks. But these attacks can occur on a daily basis up to five times a day. These attacks usually last for up to 20 minutes or so when she has these attacks, uh taking Cocodamol can ease the severity of the pain. What would be the first step in her management? Should we consider a blood test to rule out uh temporal arthritis? Does she need an urgent CT scan of the head or an MRI that would be useful? Uh Should we try new sumatriptan nasal sprays that uh uh has a foster uh action compared to the tablets? So it may have uh briefer attacks or would the course of indomethacin we have for? So this lady has a different types of headaches, which is a side locked headache only occurring in the right on the right side in the um five per one distribution. And there also there are some features of possible uh uh autonomic uh uh mm symptoms during the headaches. These headaches are also different in terms of duration of the symptoms because the the attacks only last for about 20 minutes or so. And they can occur up to uh five times on the same day. So, the combination of these features is highly suspicious of a condition called uh paroxysmal hemicrania. Uh which is another type of a uh trigeminal autonomic headache disorder. Indomethacin is the first choice for this uh headache disorder. So, just to review of the most common trigeminal autonomic uh headache disorders, these are always unilateral headaches with the trigeminal nerve distribution, which means that the headache is very rarely affecting the occipital area or the or the parietal area. More common around the eye socket and the ipsilateral cranial autonomic features that we already discussed is a is a very specific finding. These headache disorders are not well understood, especially the shorter duration attacks, cluster headaches. There is good evidence that they are related to dysfunction of the hypothalamus, which uh basically uh contains the biological clock of the brain. That's why um these headache attacks come in certain times of the day in cluster headaches, not uncommonly uh in the night hours. And uh the other headaches have different features and their pathophysiology is not well understood when you see people with cluster headaches, paroxysmal hemicrania, hemicrania continue or uh sont which is a shortlasting unilateral uh neurology from pain with conjunctival injection and uh leg cremation and the headache. Uh description is quite similar. The autonomic features are also quite similar. What is different in different. Uh these types of headaches is the duration of the attacks. So, a typical patient with cluster headaches, uh can have a headaches lasting for half an hour or up to 23 hours. People with paroxysmal hemicrania have shorter attacks and they repeat themselves up to 2030 even 40 times a day. There is a minor and more chronic version of the similar headache types, uh which is called hemicrania continua, which is a continuous fluctuating, mild to moderate unilateral headache disorder. And the extreme version of the brief headache attacks is the song where the headaches are of extreme severity. They sometimes can last only for 2030 seconds, but they can happen several times a day even up to uh every minute or so. T cluster headaches. Uh almost all of them have the orbital pain and the autonomic features and the duration of the attacks and especially that the headaches occur in the night hours usually help us uh make the the definite diagnosis in my experience. The best way to distinguish these headaches disorders is to establish the number of the attacks per day and the duration of the attacks. We will talk about the management of uh cluster headaches. Cluster headaches uh are different from migraines, but they still respond well to sumatriptan, usually the subcutaneous or nasal spray form sumatriptan tablets don't seem to make a difference because the relatively slow absorption of the medication doesn't allow to kick in uh before the headache finishes 100%. Uh high flow oxygen inhalation is also a way to help people with cluster headaches. People with paroxysmal hemicrania or hemicrania continue often respond well to indomethacin. Indomethacin is an old fashioned non steroid antiinflammatory drug. Unfortunately, there is a high risk of causing uh gastrointestinal side effects. So we usually start people on a relatively high dose and try to uh taper the dose and uh continue the lowest effective dose to help them. The brief version of uh trigeminal autonomic headaches. The soct headaches often respond that to lamoTRIgine, which is one of the epilepsy medications. So, primary headache disorders are those where we don't uh suspect an underlying medical problem or structure abnormality in the brain. And uh although these are be benign headache disorders, unfortunately, many people uh uh require medical advice or attend even hospitals or A NS because of uh severe headaches when they get out of control or they can't manage at home. People with tension headaches, very rarely see GPS or come to hospital with the headaches because they are mild and uh nonsteroid antiinflammatory drugs. Uh uh usually help those who develop chronic tension headaches or high frequency tension headaches. Uh amitriptyline or a course of acupuncture may uh help them migraine, which is the most common headache disorder that uh require medical uh uh uh attention. People who have a migraine attack and they cannot self manage non steroid anti inflammatory drugs or sumatriptan or other Triptans are the way to abort the attacks, nausea and uh severe dizziness is not uncommon. So, antiemetics in combination with the above tablets is very, can be very helpful. And uh there are many uh tablets of different uh kind that we can prescribe for migraine prevention. Unfortunately, these have very nonspecific uh effect and uh the response rate is relatively low still, we still we use them because uh uh first because most people who come to see a doctor with severe migraines are, are real, really troubled by the headaches. And uh quite often we can identify coexistent other medical problems or anxiety that can be helped with the medications that we can offer to them. Um Propranolol, amitriptyline, topiramate Candesartan pizotifen are all different uh uh medications which uh mode of action is completely different and there is nothing in common in them. These basically are experimental uh anecdotal findings uh that led to the discovery of these medications helping migraine people. For example, Propranolol and Candesartan are mainly used for BP, historically, especially propranolol because we don't use it anymore in cardiology or any other medical problems. Uh Mainly anxiety disorders and migraine. Uh the indication of using propranolol amitriptyline is an old fashioned uh tricyclic antidepressant that uh psychiatrists don't use nowadays. Uh One reason is that uh amitriptyline overdose is quite often fatal. So people with severe depression are not given amitriptyline to have uh depression symptoms. Uh Candesartan is a newer anti hypertensive medication that uh that uh I found very helpful in clinical practice. And many people fear the migraines are much better controlled on them. And the side effect profile is a profile is pretty uh uh good topiramate is an one of the epilepsy medications that is also licensed in migraine uh prevention. The way it helps migraine is not well understood. Pizotifen is an old fashioned migraine prevention drug that uh that has similar effects uh compared to mic uh triptans and uh uh but its use is getting uh less and less uh acupuncture. Interestingly is also mentioned in the nice guidelines for migraine management. But in, in everyday practice, I don't think that anybody recommends acupuncture for headache for migraine patients. So cluster headaches when the diagnosis is uh uh confirmed by a specialist. If the sumatriptan subcutaneous injections or the nasal spray is not enough to help people manage their cluster headaches. High flow oxygen can be prescribed in a portable cylinder. And uh prophylactic uh medication is the first choice is verapamil. Quite often people who suffer with seasonal episodic cluster headaches which usually uh about occurs once or twice a year, starting a course of oral predniSONE at the start of the cluster bout uh can be very helpful. I just like to quickly mention new treatment options for migraine because uh as so many people suffer with migraine, uh people in other specialties or, or uh even on the acute medical take, can can meet uh can encounter people who want uh advice on migraine management Botox copy injections is a licensed treatment for people in chronic migraine. Chronic migraine is defined as uh people who have severe migrainous headaches and uh at least 15 headache days a month from which eight is a migrainous. There is a new uh development in the last four or five years. The first uh was CGRP monoclonal antibodies. CG RP is the main chemical that is driving the the headache in migraine attacks. CGRP is a vasoactive chemical that uh that basically causes vasodilation and vasodilation in the cranial arteries basically is the mechanism of uh the pulsating headache. So CG RP monoclonal antibodies such as a va mo or mg are very helpful and uh people I met and are on these, on these injections which is mostly injections usually stop having headaches or the headaches are much more manageable. In the last few years, there has been new players on the market which is basically a tablet form of a of a similar uh mode of action drugs. The gant or vidua is a tablets can be used for acute treatment of or prophylaxis of episodic migraine and the aquita tablets can be used for migraine prophylaxis. There are also other devices such as the Guaco device which is a vagus nerve stimulator that can help people with migraine and also cluster headaches. We haven't finished with headaches. So we continue on the theme of headache disorders. This young man came to A&E with a severe headache he was in hospital two days ago with suspected viral meningitis. The CSF studies were normal now, he came back with severe pain in his neck and all over the head. When he gets out of bed, he is dizzy and feeling faint when walking these headaches uh and the dizziness ease off when he lies down. What do you think would be the best way to manage his symptoms on day one of this new hospital admission, is there any concern that he may have uh a complication of the lumbar puncture that he had two days ago? And uh has now meningitis. Should we do? A CT head? Should be just monitor him in hospital with bed rest, increased fluid intake and some pain management is an epidural blood patch indicated in this case or should we start him on or, or more? I think the best answer. Uh best res re answer is uh treat it as a post LP headache. So the patient has positional headaches which is made worse by getting up and uh eased off when lying down. And this is highly characteristic of uh what we call low intracranial pressure related headaches. The most common example of low pressure headache is post LP headaches, which is down to an ongoing CSF leak due to the uh recent lumbar puncture. In most cases, bed rest, uh fluid increased fluid intake, increased coughing intake or, or pain management can help to alleviate the symptoms over a few days, very few people require an epidural blood patch, which is usually given by an anesthetics if the headaches don't settle down and the patients are disabled, uh, with these headaches, Oramorph is a commonly prescribed drug for acute headaches, especially in, uh, in hospitals. Unfortunately, um, it can cause a lot of problems and because people, especially with chronic headaches are prone to medication, overuse headaches or, or, uh, uh, uh, because of the high frequency headaches. If you, if you use these medications, they can lead to tolerance or sometimes dependence. Opiates are not a favor drug choice for uh headache management. Uh The patient didn't have other features that would indicate another ct and repeat lumbar puncture can just make worse the post lumbar puncture headaches. So compared to the people who present with chronic or or frequent headaches and see the GP there are certain uh headaches that uh represent acute medical problems. Uh One example is uh acute uh narrow angle glaucoma, which usually starts with a severe uh visual disturbance. It can be seeing halos, visual visual impairment and uh people can have a painful red eye and also uh nausea and severe from the headaches. Thunder grab headache is a different entity. Uh This medical term is usually used for severe, often prescribed as the worst ever headache when the mm uh headache intensity reaches the maximum within a few minutes, usually within two minutes. So people who developed uh who developed severe worst ever headaches, but the headache intensity is reached uh over hours or days are not thunderclap headaches. So, when we see people with rare, so, headache, uh the most common thing to rule out is a subarachnoid hemorrhage. People with CNS infection quite often present with a severe headache. Uh In most cases, we can uh we can uh uh recognize meningeal irritation by neck stiffness or the positive sign. And uh C NS infections are almost always uh uh come with high temperature including viral encephalitis. People with sinus headaches. Uh uh quite often see other specialties than GPS or ENT. And uh we have to recognize the symptoms of sinus blockage. And classically, this patient's headaches are aggravated by putting the head down. There are certain headache disorders that come with uh uh intracranial hyper or hypotension. Uh The best example of intracranial hypotension is uh uh people with postpuncture, headaches or CSF leaks, intracranial hypertension. Uh headaches usually present with uh symptoms of raised intracranial pressure. These headaches are often position related. People who have intracranial hypertension, the headache often gets worse when lying down or coughing or straining. And people with intracranial hypotension in the early stages, they are still actively. Uh There are only when people are upright and uh disappear when going uh flat or lying down. But uh people who are not treated early with intracranial hypotension down to CSF leaks. Quite often develop a chronic daily headache, which is not position dependent. And uh when we see people with chronic daily headaches, uh but not position dependent. Often taking the history how the headache started uh points to a potential CSF leak as a cause of the headaches. People with severe or progressive headaches. Uh One thing we have to rule out is intracranial space occupying lesions. The nature of these headaches that are in they are progressive in terms of severity and how, how it affects people's life. And folk neurological deficits are not uncommon above the age of 50. Uh temporal arteritis or giant cell arteritis is also a common different when people present with new onset headaches. The nature of these headaches is always a progressive headache with scop tenderness quite often, asymmetrical headaches and raised CRP and ESR are almost uh uh uh almost always present. Although in very early stages, uh inflammation markers can be normal in the neurology outpatient clinic. It's not uh it's quite common to see people with uh symptoms of raised intracranial pressure depending on the age and other uh uh comorbidities. Uh especially if the if it happens in in overweight. Uh uh women of childbearing age idiopathic intracranial hypertension is a common cause of uh the above symptoms. These people present with po uh uh progressive headaches. Uh The nature of the headache is the possibility of intracranial hypertension as uh they get worse when people lie flat, they are made worse by coughing, bending, physical exertion and there are also other features such as transient visual obscurations, pt tinnitus photopsias, uh back pain that we often see the investigations include uh cranial imaging. We have to demonstrate that people have no intracranial tumors or other uh pathologies such as uh Crohn uh cerebral venous sinus thrombosis that can increase uh intracranial pressure. There are other features of uh uh pinpointing to idiopathic intracranial hypertension such as empty sella or uh increased uh CSF uh in the optic nerve sheets. An ophthalmology review is essential because uh in uh uh general neurologic clinics or, or people who only use an ophthalmoscope, an early poppy edema can be easily missed, missed a swollen optic disc, peripheral visual fear defects and increased blind spot on the visual fear testing is uh quite often uh uh helpful finding after uh negative uh cranial imaging and uh confirmation of PPI edema. The next step is lumbar punctures where we have to demonstrate people have raised the opening pressure. The opening pressure is something that can be easily misleading. One reason is that uh people have to be relaxed and uh and uh in the lateral that could be dispositioned to have a uh reliable measurement. And uh if the patient is tensing up or uh or there are other features like a very difficult lumbar puncture, it can also change the opening pressure. The opening pressure is also proportional to body weight. So extreme obesity can also increase the opening pressure, not necessarily caused by idiopathic intracranial hypertension. So we have to recognize the full clinic picture of I before we make a definite diagnosis. So the management of I IH is uh should be focused on weight reduction. If people are, when people are overweight, there are medications that can reduce uh CSF production. Uh These are uh acetaZOLAMIDE topiramate and uh if the conservative manners are measures are not sufficient and especially when people have significant visual impairment. CSF redirection treatment with a V patient shunt or out patient or optic nerve sheet fenestration in acute visual loss are the treatment options. Let's change topic. Now, let me just check where we are in time. Ok. A lady in her seventies was brought to hospital by her husband. They came back from a holiday a week ago. Uh They both had diarrhea when they were on a Caribbean cruise. She started having pa pains in her legs and lower back a few days before coming to hospital. And uh this morning, she was unable to get out of bed. She had slurred speech due to bilateral facial weakness and she was quite unsteady on her feet. She had quite severe leg weakness as she couldn't lift her legs off the bed. What do you expect to find on examination based on this uh clinical presentation? Uh would you, would you expect tongue fasciculations? Would you expect some nystagmus joint position sensation because she's unsteady on her feet? Can it represent uh some peripheral neuropathy. Would you expect the reflexes to be present or not? And uh and uh would you rec uh would you suspect some uh C NS pathology that can uh come with upgoing plantas? So, the most likely uh cause of this presentation is Guillain Barre syndrome were uh quite often following an infection such as diarrhea or illness or uh uh chest infections or viral infections. Uh People have symptoms of ascending weakness, usually starting in the lower limbs, pain in the lower back and the legs is not uncommon in uh Guillain Barre syndrome. And uh sometimes it can be a misleading uh thing and uh point to some spinal pathology and as she has severe weakness in her legs, she cannot lift her legs off the bed. Um You would expect that the neurological examination would help you understand whether there is any upper or lower motoneuron uh deficit. So, diffuse a reflex here is what you would expect in Guillain Barre Syndrome. Um people with upgoing plantar cannot uh avoid having an MRI scan of the spine because uh corticospinal tract involvement or spinal cord pathology is very rare in uh Guillain Barre syndrome. Although some people have uh overlapping symptoms with uh with uh acute spinal cord lesions when they have Guillain Barre Syndrome. For example, sphincter abnormality, occasionally upgoing plantar responses uh can be seen in guillain-barre patients. But by and large, uh people have an ascending leg and later arm weakness. Quite often, the weakness can spread to the facial muscles or the bulbar muscles, affecting swallowing and speech. It's not uncommon that people with guillain-barre syndrome report sensory disturbance, mainly numbness or pins and needles, but uh joint position sensation is not affected by guillain-barre syndrome. So, as we know that Guillain Barre syndrome is a rare acute post infections, immune mediated polyradicular neuropathy. Yeah, I'd like to highlight this is a poly radicular neuropathy which means that the pathology involves the nerve roots and the more distal sections of the peripheral nerves. Uh some features can be quite misleading in Guillain Barre syndrome. For example, one feature is that uh people often present with proximal leg weakness that uh especially in Children can manifest in hip pain and uh painful movements of the hip and uh and uh that can delay the diagnosis. But most people who have Guillain Barre Syndrome, this is a rapidly evolving ascending mot or weakness with very mild sensory loss. The motor weakness can also involve the respiratory and the bulbar muscles. And uh aflexia is expected. In most cases, some people have urinary retention. It's very difficult to know whether this is down to spinal cord involvement or the acute uh peripheral nerve uh damage, affecting the uh bladder, uh nerve supply. And uh back pain is not uncommon in the Guillain Barre syndrome as well as as I mentioned, uh proximal leg weakness, possible triggers to Guillain Barre syndrome is either diary a the classic the cause is a Camp Campylobacter Jejuni inject infections and most cases especially the severe childhood form, which is the acute exon or motor neuropathy AMA N form of Guillain Barre syndrome is uh uh quite uh common in uh in China. So the biggest descriptions of uh of this uh epidemics of uh Guillain Barre syndrome came from China and uh affected mainly the pediatric population. Other infective causes include mycoplasma EBV CMV infections and uh also post vaccination. Guillain Barre syndrome was reported. So, Ma Guillain Barre syndrome, uh there are quite a few challenges to make a definite diagnosis of guillain-barre syndrome. Ideally, people should have nerve conduction studies that can demonstrate the segmental demyelination or exon or loss affecting the nerve roots and the distal part of the peripheral nerves. There are two challenges. One challenge is that in most hospitals, nerve conduction studies are not available as an urgent test. And in peripheral hospitals like in Kingsmill Hospital, we don't have nerve conduction studies. And the other difficulty is that the findings of nerve conduction studies start to appear at least after one week from the onset of the symptoms. So when people present uh to hospital with suspected Guillain Barre syndrome, we don't have a week or so just to have a diagnosis. So we have to make a diagnosis based on the clinical presentation. And another feature that can help is the CSF studies as there is acute uh pathology in the, affecting the nerve roots. Uh It comes with a breakdown of the uh blood uh uh CSF barrier that uh that can cause elevated protein levels. But uh because this is a post infectious uh autoimmune disorder driven or uh mediated by antibodies, not with cellular uh immune uh reactions. The usually the CSF cell count is normal. So this dissociation uh uh in the C CSF with elevated protein and normal cell count is the characteristic finding in CSF. Unfortunately, the CSF studies can be also misleading. So it's not uncommon that on the first day or two people who don't have the most severe form of Guillain Barre syndrome, the CSF protein can be normal. So we have to see the full clinical picture. And if you find someone with acute onset, progressively worsening motor weakness, especially with aflexia and no signs of upper motor neuron involvement like uh extensor plantar response. Uh The Guillain Barre Syndrome diagnosis can be confirmed on clinical grounds and we should start treatment. The treatment should be given as early as possible because delayed treatment would basically reduce the chances of good recovery for the patient. This antibody mediated immune response is basically attacking, damaging the nerve roots and the nerve uh the peripheral nerve uh fibers in the classic form of Guillain Barre. It's mainly demyelination that occurs, but there is one severe form. Uh the acute exon motor form of uh Guillain Barre syndrome where the distal axons are the main target for the antibodies. And uh it's an acute axonal loss in the peripheral nerves that is driving the symptoms. There is another variant which is very rare. But when you see one, you will never forget, these are the patients with uh Miller Fisher syndrome. Uh The classic triad of uh Miller Fisher syndrome is aflexia ataxia and ophthalmoplegia. So, the extraocular muscles are also involved in this. And uh there is a specific antibody test that can confirm this uh uh subtype of Guillain Barre syndrome. It's the anti GQ one B antibodies. Again, in everyday clinical practice because it takes ages to get these antibody results back. Uh This is just, this just helps us to confirm the diagnosis later in the course of the es but the decision making on day one of the I is should be, should rely on the clinical presentation, identifying the possible triggers like a recent infection. Uh It's quite helpful to have the CSF protein but a normal CSF protein with a with a high clinical suspicion doesn't, shouldn't uh put our put us off uh starting treatment. So the treatment is usually plasma exchange which is limited in uh many hospitals, usually hospitals where there is a renal unit. Uh plasma exchange is available in most hospitals, we use intravenous immunoglobulin treatment. So, Guillain Barre Syndrome has highly specific uh features which usually help us uh uh confirm the diagnosis. But still there are other uh medical problems that can cause quite similar presentations. For example, uh acute transverse myelitis, which is a form of a, yeah, autoimmune inflammation in the central nervous system, acute transfer my transfers myelitis quite often is a postinfectious myelitis caused by uh certain uh viruses. Uh but autoimmune uh transverse myelitis uh related to certain antibody mediated disorders can also happen. The one feature of this is a usually more abrupt onset of motor paralysis in the lower limbs. And there is a sensory level which represent the diffuse uh uh spinal cord inflammation, not limited to the motor, uh nerves botulism is more of a textbook textbook example because uh uh it's very rare to see people who suffer with botulism. Uh botulinum toxin uh is uh a form of uh uh food poisoning which uh which can be related to eating rotten food. So that's why that's why it's not common. It can happen sometimes in people who are alcoholics or homeless people who who get access to some rotten food and they eat it. And uh descending paralysis usually starting in the cranial uh muscles or the upper limbs going down to the legs. Uh having apoptosis compared to gum body where uh eyelid muscle weakness is not common or doesn't occur. And the fixed pupil uh which is a a very helpful finding in botulism can also distinguish it from Guillain Barre Syndrome. People with acute spinal cord compression sometimes present with an acute ascending paralysis starting in the lower limbs. But uh almost everyone with acute cord compression have abnormal plantar response and uh pain, localized pain in the spine is also uh pointing to acute spinal pa pathology. Uh for example, people who have metastatic cancer spread to the spine causing acute cord compression, uh nerve irritation pains, radicular pain and severe back pain is uh almost uh uh almost always present. There is another type of demyelinating polyneuropathy. It's called uh chronic inflammatory demyelinating polyneuropathy. C IDP, which is a subacute progressive form of uh immune mediated demyelination in the peripheral nerves. And when people have a uh insidious onset of this leg weakness or other symptoms in CIDP and they end up in hospital when the symptoms suddenly get worse, it can be mixed up with Guillain Barre. But one feature uh that always helps is the progressive nature of CIDP, which usually uh the symptoms are getting worse over a longer period than two months compared to Guillain Barre, which is an ACU TNS where uh most patients reach a plateau of the symptoms within days or not later than within a two or three week period. So, if the symptoms are getting worse over two months, it's more likely a a chronic inflammatory demyelinating polyneuropathy, not Guillain Barre syndrome. There are many neurological disorders where patients experience progressive decline in walking and cognition. Uh uh when it comes to cognitive impairment, uh we expect these disorders to affect the uh older population, although some of them can also affect people in their thirties or forties. So the most common form of uh of uh neurodegenerative conditions which uh present with a progressive decline in walking and cognition is idiopathic Parkinson's disease, idiopathic Parkinson's disease quite often present with the symptoms many years before the illness. That can be highly characteristic in retrospect. One of them is uh sleep disorders. Uh rem sleep disorders are not uncommon. Uh The vivid dreams, nightmares or acting out during sleep when people are diagnosed with these sleep disorders. Uh it's basically a verdict that predisposes them to Parkinson's disease is so so characteristic. Another interesting feature in Parkinson's disease is uh loss of smell sensation. This uh represents uh the pathology usually starting uh in other parts of the nervous system, not in the motor nerves or the basal ganglia. So, non motor symptoms, especially the sleep disorder or the loss of smell sensation. Uh quite often the first symptom of Parkinson's disease. Parkinson's disease is not only limited to the dopamine system. This is a multisystem disorder of the central nervous system. And the other features such as urinary symptoms or low mood depression can, can be the first presentation. So most people are diagnosed with Parkinson's disease when they develop the motor symptoms, which is usually characterized by decremental brody kinesia almost in every case uh occurring in one hand, first only and uh increased muscle tone uh with the typical cochlear rigidity is what we expect to see in a patient with a Parkinson's disease. And brody is in the hands, tremors are characteristically unilateral first and uh uh uh present at rest. So the rest tremor, the brody kinesia and this uh tone increase with cochlear rigidity is what we see in most patients with uh Parkinson's disease. So the pathological changes in the brain usually start in one part of the brain and then slowly spreading across the brain. That's why the symptoms always start in one side. So, the unilateral onset of the symptoms is is highly characteristic in Parkinson's disease. Parkinson's disease is a diffuse brain disorder. Unfortunately, many people have uh uh developed Parkinson's dementia or cognitive impairment. It's not typical in the first year of Parkinson's disease. So, if the cognitive decline starts in the very early stages of Parkinson's disease, we have to think about other conditions that present with some symptoms of Parkinson's disease. I mentioned that urinary symptoms like urinary urgency or incontinence is not uncommon in Parkinson's when the symptoms spread and uh become bilateral, like affecting both sides of the body quite often. Uh uh it affects walking and balance. The typical shuffling gait and reduced arm swing is uh is very easy to recognize during the examination. So when we see people who have progressive walking, difficulty and cognitive impairment, uh one condition that is treatable is uh normal pressure, hydrocephalus. These people usually in their fifties or sixties. It can occur in men and women. And uh not uncommonly, they had some brain disorders uh previously such as previous uh head injury, strokes, subdural hematoma, which somehow affects the resorption of the CSF. And uh this uh leads to a fluid expansion in the lateral ventricles mainly or the ventricular system. And also the, the cortical cell side can be widened. So these changes on the brain can cause different uh uh impairment of function. Typically, these patients have a wide based magnetic gait, which means that they have difficulty lifting the feet off the floor. Uh It is different from the shuffling gait. What we see in Parkinson's disease. It can also cause global uh brain dysfunction with reduced attention span, reduced concentration, problem solving and later memory difficulties. And another feature we often see is urinary urgency and frequency progressing into incontinence, hydrocephalus is the hallmark uh for the diagnosis. So you, you should see significant uh ventricular enlargement in uh normal pressure hydrocephalus and no significant cortical atrophy. Another condition that is very common, especially with increasing age is Alzheimer's disease. So, Alzheimer's dementia uh usually presents with short term memory difficulties, often followed by more global cognitive impairment and uh gait apraxia later um neurological deficits or uh neurological signs of uh global brain dysfunction such as uh uh gait axia, other grade disorders, ataxia or uh upper motor neuron signs is not uncommon in Alzheimer's disease uh compared to the normal pressure, hydrocephalus. Uh brain imaging often shows cortical atrophy and especially hippocampal volume loss. Uh That is a distinctive feature of Alzheimer's disease. There's another type of dementia that can cause uh walking and cognitive dysfunction. This is the vascular dementia. So, vascular dementia usually develops in people who have had significant cerebrovascular disease with multiple strokes. And as a result of the strokes, they have stepwise deterioration in neurological function, focal neurology on examination and uh focal changes with cerebral infarct on brain imaging point to advanced cerebrovascular disease. Other rare forms of progressive decline uh include uh prions disease like CRE ob's disease. But usually the presentation is more uh dramatic with very rapid onset dementia. Usually within a month or two people have significant uh cognitive dysfunction which make them uh unable to live an independent life. And uh there are other features which we often see such as myoclonic jerks or uh cortical blindness that we see. So certainly the presentation is completely different from Parkinson's or normal pressure hydrocephalus. But uh in early stages, it can be mixed up. So if we look out for early symptoms of uh unusual cortical dysfunction, like myoclonic jerks or uh or visual field impairments or cortical blindness, uh that can lead to a diagnosis of uh prions disease on the theme of Bryan's disease, which is uh uh uh uh devastating illness. Uh uh Let's see an example of patients with Huntington's disease. Uh The patient came to A&E following a fall. He had a previous diagnosis of Huntington's disease. He lives in a care home and he wasn't coping because he wasn't coping at home. So this probably means that he has the advanced, uh, he's in an advanced form of Huntington's disease. What are you expecting to find on neuro examination? Uh, do people with Huntington's have an extensor plantar response, vertigo, nystagmus, fasciculations, chorea or facial weakness. It's quite obvious that uh chorea is the answer here because uh Huntington's disease is a condition which often presents with chia movements. Uh Mood changes, usually depression, cognitive difficulties, later this artery or ataxia swallowing difficulties. This is a genetic disorder, uh showing uh Atal dominant pattern. So the positive family history is almost a prerequisite for the diagnosis of Huntington's management of Huntington's patients. Uh uh is challenge, uh full of challenges. And uh in the advanced uh stages of Huntington's disease, we have to make decisions about feeding and end of life and an advanced care decision when people are still able to make a decision. And uh a lasting power of attorney would really help the management around these issues. There are other relatively rare genetic disorders that quite often uh present in neurology. One of them is uh tuberous sclerosis, which is a multisystem genetic disorder. Uh In my experience, these people usually are referred to epi uh neurology with epilepsy and uh, they almost always have some intellectual disability, the facial tumors the angiofibromas are uh are the hallmark of disease. And uh quite often these uh benign tumors affect the kidneys and uh many of them uh end up having uh kidney transplants in the last 10 years or so. Uh There has been a drug available to slow down the progression of the CNS is everolimus, which usually is prescribed to people who have significant renal impairment or difficult to control. Epilepsy. Friedrich ataxia is the most common hereditary ataxia. Uh The symptoms usually start in teenagers with a slowly progressive cerebellar dysfunction, uh kyphoscoliosis and quite uh often they are found with hypertrophic uh hypertrophic obstructive cardiomyopathy or diabetes. Uh Let's change topic. Now, a man in his sixties is brought to hospital with severe ataxia. He's a heavy drinker and according to his family, he didn't leave the house and didn't have a meal for the last three days. His blood sugar was quite low when the ambulance arrived. What are you expecting to find during the assessment in A&E? Uh would you expect uh hypothermia, uh limited eye movements, uh confusion or all of the above. So, this clinical presentation uh solder onset ataxia in a heavy drinker who hasn't been eating well, is quite a uh suspicious of Wernicke's opathy. So, Wernicke's encephalopathy is an acute uh uh basically a life threatening emergency, which is down to acute uh thiamine deficiency. So, thiamine is a vitamin that is uh essentially in the carbohydrate uh metabolism and uh people who have sudden large amount of uh carbohydrate intake can be relatively deficient on in thiamine and those people who are not eating well, uh let it be down to alcohol abuse, uh prolonged fasting, severe diarrhea, uh recent bariatric surgery or uh uh pregnant women who uh with hyper MS uh are all prone to uh thiamine deficiency. So, thiamine deficiency can cause acute uh brain damage. The typical symptoms are affecting the eye movements. So, quite often people have a limited uh horizontal gaze with the nystagmus. Uh they are very unsteady on their feet. This is down to acute uh cerebellar dysfunction and uh they have cognitive impairment, mainly confusion. The treatment is parania, amine for uh five days, followed by oral thiamine and uh nutrition review. So, in this case, his blood sugar was low. If you, if you treat this with uh with IV glucose or uh gluco, uh there is a high chance that you make the wernickes worse because the Wernicke encephalopathy is down to acute thiamine deficiency and uh sugar intake basically increases the demand of thiamine. So if you give sugar to a patient without thiamine supplementation, it can make the situation worse. So it's essential that you supplement the thiamine before you, you correct the hypoglycemia unless people need uh have a acute hypoglycemic episode. Uh So in this patient group, uh mainly uh people who are a uh who have alcohol dependence, there are other conditions which can present exactly the same or severe very similar symptoms. One of them is uh acute alcohol withdrawal syndrome with delirium tremens. Uh One interesting finding is that uh most people with delirium treatments have a high temperature. Whereas people with uh Wernicke encephalopathy usually have low temperature and the low BP hepatic encephalopathy, which uh also can occur in people with alcohol dependence. Uh uh can present with confusion and ataxia uh serum ammonia is always or almost always raised. As I told you, Wernicke's encephalopathy is a is a emergency and life threatening condition. Uh Very few people make a good recovery uh from Wernicke's encephalopathy unless the treatment started very early. And uh and uh there are no other complications. Uh So many people continue to experience severe cognitive impairment following Wernicke's encephalopathy, which is uh called Korsakov syndrome. So, Korsakov syndrome is caused exactly by the same uh acute thiamine deficiency, but the damage is so severe that they never recover from the cognitive impairment. So, quite often these people develop uh a very uh severe cognitive impairment with inability to consolidate any new information. They have very severe short term memory difficulties that they try to compensate with confabulation and uh apathy and poor insight is also common. Uh in my experience, most people with Korsakoff Syndrome, if they don't have good family support, end up in a nursing home or a care home because they wouldn't cope on their own. Let's talk about other uh interesting neurologic disorders. Myasthenia in general is a condition when people have a fluctuating and uh and uh fatigue, muscle weakness. The classic example is the autoimmune myasthenia gravis, which uh occurs at any age even from uh uh from uh newborn babies. Because Children who are born to mothers of myasthenia with myasthenia gravis can have neonatal myasthenia from the circulating antibodies. But uh typically, uh myasthenia affects uh young adults uh who are prone to autoimmune disorders. And there is a second peak in the the population around the age of 70 or 80. Uh so, so late onset myasthenia gravis is also an autoimmune disorder which uh which we often see. So, autoimmune myasthenia gravis uh presents with fluctuating muscle weakness and fatigue. This is down to circulating antibodies in the blood stream that uh uh cause damage uh in the muscle and plate. The most common antibodies that we see uh is called receptor antibodies and musc uh muscle specific kinase antibodies. So, these antibodies uh cause uh damaging the nerve, uh uh muscle and plate, which basically reduces the uh the efficacy of the neuromuscular junction. So, this reduced efficacy in the neuromuscular junction via result in a fluctuating muscle weakness and tiredness. The muscles get tired and those muscles which have very small number of muscle fibers are more uh prone to the uh myasthenia fatigue. That's why those muscles that are very small, like the ocular muscles, the bulbar muscles are often uh uh involved in the early stages of myasthenia. So, the typical patient with autoimmune myasthenia gravis reports, uh fluctuating eyelid, droopiness, double vision, the voice going nasal or weak. They have dysarthria and dysphagia. These symptoms are more likely to occur by the end of the day and quite often they are not present first thing in the morning because the muscles, uh, muscle symptoms get better with resting. I recently saw two patients who self manage myasthenia with a, with a planned resting during the day, which means that uh quite often self management without any immune suppression treatment can be successful. So people who who pace their activities or try to avoid potential triggers that can make the muscle tiredness worse, can manage it without any drug treatment. But having said that myasthenia is in most cases, is a progressive disorder that can lead to life threatening complications. So, medical treatment is essential in most cases to avoid uh uh me uh emergencies with the breathing or swallowing troubles. A relatively common finding in the autoimmune. Myasthenia gravis is an enlarged thymus gland. So we know the thymus gland is part of the immune system. The cellular immunity depends on the thymus gland. It is quite large in the, in the uh before birth and in the newborn baby. And uh it's slowly getting uh smaller and smaller as we age. By the age of 25 most people have a degenerate thymus gland. So there is not much activity in the thymus gland. Some people develop tumors in the thymus gland called a thymoma. So people with a thymoma are also at higher risk of developing myasthenia. So the treatment of myasthenia is uh the first line treatment is usually pyridostigmine, which is a medication that can, that increases the acetylcholine level in the neuromuscular junction if it doesn't help enough, uh uh we have to give immune suppression. PrednisoLONE is the first line drug for immune suppression, which uh in many cases can help stabilize the condition. The main problem with predniSONE that it has a lot, lot of long term side effects and uh including uh fluid retention, hypertension, diabetes, osteoporosis, and uh many others. And the other problem with prednisoLONE that uh usually the dose that is required to control the myasthenia symptoms is quite high. But if we start the dose, if we start at a high dose straight away, quite often, the myasthenia symptoms can uh can get worse in the last in the 1st 23 weeks. So usually it's a slow escalation of the treatment that is safe to do as an outpatient. People who present with severe myasthenia symptoms when the respiratory muscles or the bulbar muscles are involved. Quite often, they need hospital admissions and urgent treatment. It's either plasma exchange or intravenous immunoglobulins. Um There is good evidence that uh removing the thymus gland, even that if there is no enlargement of the thymus. Uh can reduce the need for long term immune suppression. So the people go into remission. But certainly in most cases, if the thymus gland is not enlarged or there is no evidence of a tumor in the thymus gland, thymectomy is not recommended. So we rely on medical treatment. People who require high doses of prednisoLONE uh to maintain good symptom control. We like to use other immune suppressants to use as a steroid sparing agent such as azaTHIOprine mycophenolate mofetil. There is a other form of myasthenia, which is called Lambert Eaton syndrome. Just sorry. I'm just checking the time. Lambert Eaton syndrome, which is a paraneoplastic autoimmune disease. In most cases, the Lambert Eaton syndrome doesn't really present with myasthenia specific symptoms. So the usual ptosis and double vision or nasal voice is can happen or can occur. But these people usually present with lingered weakness, like weakness in the legs. The proximal leg muscles is a common common presentation and they have some autonomic symptoms such as dry mouth and difficulty uh micturating. So the presentation can be completely different. Uh certain tests like an emg neurophysiological assessment can show characteristic uh postactivation facilitation, which means that the muscle fiber contraction is getting stronger with the, with the, with the repeated contraction. Whereas in auto in myasthenia gravis, the with increased contraction of the muscle fibers, the day gets weaker and weaker. So this is the opposite of what we see in lumbar syndrome. There is a facilitation of muscle contractions with activation. Whereas in myasthenia gravis, there is a decrement which means that uh the muscle contractions are getting weaker and weaker on repeated uh uh contractions. Lumbar T syndrome is most common in small cell lung cancer patients. But there are also cases of uh pure autoimmune uh forms compared to the typical myasthenia antibodies. The sat calling receptor and MOSK antibodies. Uh many patients with lumbar T syndrome, uh we can find voltage gated calcium channel antibodies which are basically uh binding to a presynaptic uh calcium channel in the uh nerve endings that basically uh affects the release of the act according into the uh neuromuscular junction lumbar T syndrome. Uh can be helped with uh a tablet, a drug called uh 34 diaminopyridine. Uh but uh treating the underlying cancer is the only way to have these people. But I just like to briefly touch on the MS. Uh multiple sclerosis uh has developed the management of sclerosis has developed so much lately that it has become a highly spec specialized uh subspecialty in neurology because there are so many other, so many treatment options are available that uh that uh MS uh management is not possible in general neurology or rehabilitation services. So, uh as a general neurologist, I don't have much exposure to MS patients these days. So I just like to briefly touch on the MS MS is relatively rare disorder. Uh Although for example, in the UK which is a high altitude country. Uh This is more common. Uh One in 400 people are at risk of developing MS. In general. Multiple sclerosis is an autoimmune disorder. It's a chronic cell mediated autoimmune disorder. So, there are no antibodies in the blood stream that you can detect to diagnose MS. And uh it causes inflammatory demyelination in the CNS. Uh You can see this uh a sagittal view on a flare uh sequence of MRI that shows uh in the corpus callosum, this uh finger like uh uh uh hyperintensities. These are called the dorsal fingers which uh represent uh inflammatory demyelination. So, MS can present uh with a different uh uh vase. Most people who develop, MS have the relapsing, remitting form of MS uh which affects 85% of people. Uh This uh patient group usually have relatively mild symptoms in the first few years. Uh Quite often the symptoms can be uh uh an episode of optic neuritis or sensory disturbance or spinal cord inflammation from which they spontaneously recover within a few weeks. And uh between MS relapses. These patients are quite often completely symptom free and fully independent. Some of these patients over the years developed what we call secondary progressive MS, which means that after sever relapses, people start to develop some chronic disability, which is slowly getting worse over the years. Very small number of cases uh in MS uh start with primary progressive uh uh symptoms which means that the symptoms never come as a dramatic uh relapse but slowly progressive symptoms. Uh uh um are, are the feature somehow it is more common in men of middle age rather than the young ladies in, in uh in their twenties or thirties, which is the most uh common common uh in uh in relapsing, remitting MS. And quite often people with primary progressive MS start with the spinal cord symptoms when people have their first presentation of MS symptoms. Uh We use this term clinically isolated syndrome to distinguish it from uh uh a definite diagnosis of MS. People with the, with the first presentation of CNS inflammatory demyelination quite often, uh have a one of uh presentation and don't develop into a turn into MS uh later in life. So, multiple sclerosis quite often present with a visual disturbance, uh optic neuritis or uh uh jumpy or wavy eye movements, uh quite often caused by internuclear ophthalmoplegia or double vision. Uh There are many symptoms that uh can overlap with many other conditions or or or life experiences, for example, increased fatigue, depression, cognitive impairment. Uh So as A MS is quite a publicized uh medical problem and uh and uh having the fear of MS uh pushes many patients who have chronic fatigue, depression or cognitive impairment for different reasons to ask for investigations to rule out MS, pain or sensation is also common in MS. There are certain things which again are difficult to distinguish from other problems. Like many people who have spinal cord inflammation, experience chest tightness or water sensation on the trunk. Trigeminal neuralgia, which is considered to be uh an isolated trigeminal nerve uh irritation usually from uh blood vessels, uh is also not uncommon in MS. So, if you see trigeminal neuralgia symptoms in a young patient, like below the age of 30 it is quite likely to be related to MS because trigeminal neuralgia usually affects uh middle or older age patients. There is also this classic LMIT phenomenon when head flexion can cause uh nerve irritation symptoms or uh or pains or pins and needles or paresthesia down the spine. Uh This is not uncommon in a spinal problem. So it's also quite specific if uh if uh if you find it in the right context, spasticity in the muscles down to previous uh CNS damage is not uncommon in MS, especially in the progressive form of MS. And uh as spinal cord involvement is quite common in later stages, bladder and bowel dysfunction or sexual dysfunction is also common. So, when we see people with presenting with different uh neurological symptoms, some of them are, are specific uh or quite common in MS like optic neuritis or internuclear ophthalmoplegia. Unfortunately, many patients who present with nonspecific symptoms like chronic fatigue or depression. Uh we need, we need some tests to, to uh uh basically to rule out other medical problems. Uh a full, full battery of blood investigations to rule out common medical problems that can cause many of these symptoms such as underactive thyroid or vitamin b12 deficiency, iron deficiency anemia, chronic liver disease, uh has to be ruled out before we consider MS the MRI brain and spine is the most specific uh uh or mo most useful diagnostic test. There are certain criterias which we have to follow the 2017 mcdonald's criteria, which basically helps us understand all these white blobs on the MRI, the localization and the number of these lesions uh basically have the diagnostic process. People who have classic uh clinical presentation and highly suspicious MRI for MS uh don't necessarily need CSF examinations. But if the MRI is not helping enough to make a definite diagnosis, finding uh oligoclonal Benz and to rule out other C NS uh pathology is quite helpful. What we have to understand that MS is a progressive MS. So what we have to demonstrate before making a definite diagnosis of MS is the dissemination of MS blocks in time and place. For example, if someone has a first presentation of MS with optic neuritis, and we see four areas of demyelination on the brain scan, uh we can make a diagnosis of MS because the optic neuritis doesn't necessarily show up, show up on the brain scan and the four demyelination blocks mean that it has been or uh this patient already had MS process uh before. So the dissemination in time and place is guaranteed. This patient has secondary progressive MS and uh, she's complaining of severe fatigue symptoms. She can walk with a stick but she gets tired easily and her muscles ache, uh, after a short walk, she takes aspirin and atorvastatin following a heart attack. Uh, and uh, the GP wanted to make sure it's not a statin side effect. So her serum CK was normal. Uh She asked the, the doctor if we can recommend any treatment to help her fatigue symptoms. Uh What would be your first choice? Would you recommend a CBD oil Baclofen, pregabaline, amantadine or Modafinil. My first choice would be amantadine, not because it's recommended by nice uh for MS related fatigue as a first choice, but also because uh this patient had a heart attack and Modafinil, which is another choice uh can increase BP. So it's quite a dangerous treatment in people who have also ischemic heart disease. Uh Many people self medicate with cannabis or uh CBD oil which uh can help muscle stiffness, anxiety, depression. Uh I'm not sure if it helps fatigue. Baclofen is mainly used in uh MS spasticity. Pregabalin is a drug that can help epileptic seizures and neuropathic pain but not fatigue. And one possible side effect of pregabalin is tiredness. So it wouldn't be a good choice for a patient with chronic fatigue. The treatment of MS for the general uh medic or, or general neurologist is basically to treating the relapses. So if somebody comes to hospital with a known diagnosis of MS and they have uh highly suspicious uh presentation for acute relapse, we either give them IV met prednisoLONE 1 g for three days or if they can be sent home, we give them oral met prednisoLONE five mg for five days. Uh People who have chronic uh progressive MS uh and uh bladder weakness quite often a uti can uh can mimic the symptoms of a relapse. This is called a pseudo relapse. So people who have pseudo relapses, it's either a uti or, or a fluctuation of chronic symptoms that can cause uh pseudo relapse uh presentation. So in uh we have always have to make sure it's a true relapse, especially not, not the symptoms are not caused by an infection where oral steroids would not have the recovering from the infection. Uh This is modifying treatment for relapsing, remitting MS or secondary progressive MS is available. These are highly specialized uh treatment and uh assessment and decision making requires a lot of expertise. So uh it, it doesn't uh uh affect uh the general medical audience for decisions. However, we see many people who don't have access to regular specialist review and they end up seeing the GP or, or uh uh brought to hospital with MS related symptoms for MS spasticity. Nice recommends uh baclofen and gabapentin for MS related fatigue. Nice recommends amantadine Modafinil and if there is any associated uh mood disorder or anxiety. SSRI s just a brief touch on neuropathic pain. Uh neuropathic pain is a pain modality that we often relate to uh neurological disorders. Although neuropathic pain is a universal pain that can cause uh that can be caused by post surgical scars, uh spinal uh degeneration and uh the most common example is a painful diabetic neuropathy or post herpetic neuralgia. Trigeminal neuralgia can also cause neuropathic pain. And uh it's also not uncommon in people who uh had strokes, multiple sclerosis or spinal cord injuries. The features of neuropathic pain is slightly different from uh uh musculoskeletal or other uh v of pains. Allodynia and hyperalgesia are common uh features. The treatment of neuropathic pain often is uh medications, um amitriptyline, uh gabapentin, pregabalin, DULoxetine, uh uh in localized neuropathic pain, copsy icing cream, uh uh can be tried and uh and uh carBAMazepine or other uh sodium channel blocker, anticonvulsant can be helpful as well. So I'm slowly running out of time. So I will speed up a little bit and II may jump a few uh skip a few slides. So, cerebrovascular disease presents with neurological symptoms, but it's basically not really neurology who deals with it. It's uh a stroke medicine. Uh People with a suspected tia, the usual treatment is uh aspirin 300 mgs daily until they are reviewed in the TIA clinic. And uh uh we take it from there. People who have a confirmed tia or minor stroke, uh dual antiplatelet treatment with a combination of clopidogrel and aspirin is the recommended treatment. Uh if there is no significant uh risk. Uh for example, recent gi bleeds, uh clopidogrel resistance or recurrent strokes on clopidogrel is not uncommon. And uh another way to have these people is using TICO uh in combination of aspirin uh following a tia uh agre has licensed mainly in ischemic heart disease uh up to a year or so and uh it's not really licensed for stroke. Uh still uh it is increasingly present in the local guidelines. Uh Historically, before we had uh clopidogrel and ticagrelor aspirin and dipyridamol in combination was also an uh a way of escalating antithrombotic treatment. Nowadays, we don't really use dipyridamole. Although this is still an option for people with uh clopidogrel resistance. People are who are suffered a ti or minor stroke and they are found with atrial fibrillation. Uh A doac or Warfarin would be the treatment for stroke prevention. Uh Probably I skipped the acute stroke management. Uh because of shortage of time. I'd like to mention though uh subarachnoid hemorrhage, which is a common suspicion in people who are present with acute onset headaches or, or a blackout epileptic seizures and uh and uh f neurology, as we all know, subarachnoid hemorrhage is a severe life threatening. Uh illness with bleeding into the subur of no, it's place. Uh most people uh with significant subarachnoid hemorrhage have a ruptured cerebral aneurysm there are other rare causes of uh subarachnoid hemorrhage, like atrial venous malformations, uh aneurysms from uh from uh infective endocarditis or traumatic uh subarachnoid bleed. I just like to touch on the, the diagnostic process uh in A&E or on the acute medical take. So the non contrast CT head is the most sensitive way to pick up subarachnoid hemorrhage, but it's only sensitive in the first six hours of symptom onset. So, if patients present uh uh had a delayed presentation, not within the first six hours and the CT is normal, uh we have to do other tests to, to uh make sure we don't miss some arachnoid bleed, which would be the lumbar puncture. The CT is so sensitive in the first six hours that if patient presents early and the CT is normal. Uh We have to consider an alternative diagnosis like a CS infection or a or a uh a severe migraine. For example, that is an interesting dynamics of uh the time and the diagnostic test because the CT scan is more sensitive in the first few hours. But the lumbar puncture is most more sensitive if you wait at least 12 hours from the symptom onset when doing the LP. So the lumbar puncture is usually recommended in people who have a normal CT. Uh and uh and we still suspect subarachnoid hemorrhage and we have to wait at least 12 hours from the symptom onset. The reason for this, that the the degradation uh product of hemoglobin is bilirubin. And uh the bilirubin uh only appears in the CSF in uh in vivo. So if we, if we take CSF S for patients who already died or, or a traumatic uh uh lumbar puncture where, where blood got into the CSF uh uh during the procedure, bilirubin usually is not present. So the ele elevated bilirubin in the CSF, which is called xanthochromia, uh basically is highly uh suspicious of or basically confirms the diagnosis of subarachnoid because other blood uh breakdown products in the CSF, like the uh desoxy hemoglobin or met hemoglobin, uh uh can also develop in in vitro, but the only in vivo product of hemoglobin is bilirubin. So when they confirm subarachnoid bleed, either with a CT or uh a lumbar puncture, uh we need to do a CT angiogram to rule out a ruptured aneurysm. Tiny aneurysms don't necessarily show up on a CTA because uh of the vasospasm at the, the acute stage of a subarachnoid bleed can make the aneurysm appear smaller. Uh If we have a strong suspicion of uh and aneurysm or bleed, we have to discuss it with neurosurgery whether the patient needs a uh A D SAA digital substraction. Uh angiography, which basically is the most accurate test to, to show up uh tiny aneurysms, subarachnoid hemorrhage is a medical emergency. And the risk of rebleeding is the highest within 24 hours. Um as we know half of the patients who have a subarachnoid hemorrhage die from the first hemorrhage. But the risk of uh if they rebleed, usually it's fatal. So it's we have to do everything to get these people to the treatment uh as soon as possible. Just a brief uh uh touch on head injuries. So, head injuries are not uncommon and uh the most important uh thing is to, to uh identify those patients who have severe head injuries that require any urgent uh surgical treatment. The best way to communicate the severity of uh brain injury is the Glasgow coma scale. So, so the G CS is a good measure of uh con level of consciousness related to the to the head injury. I just wanted to show you a few examples of uh uh hemorrhagic uh uh uh changes on brain scans. So on the left, you see uh an example of subarachnoid hemorrhage where you can see blood pooling in the basal cisterns of the brain and also in the south side uh where you see the most uh largest amount of blood usually that is an indication of the locality of the aneurysm. In this case, it's probably aic aneurysm on the left side in the middle, you can see a case of an epidural hematoma which has the typical lentiform shape of the blood collection. And you can also see the the impact to the head which uh which uh for uh with the scarp hematoma and uh epidural hematoma is usually uh uh caused by fractured scar fractures and uh rupture of the meningeal artery suba hematoma. Uh it is quite a tricky uh condition because many people have subacute or chronic presentations. And also the symptoms can be very mild and all of a sudden can cause sudden deterioration and death. So, the the classic uh feature of a sub hematoma is this uh uh crescentic uh appearance of blood collection in the acute stage, which uh if it's large enough, it's causing midline shift and uh and herniation, let me just check where I am. OK. I have a few more minutes. So, monocular visual loss uh if we are lucky, uh these patients are not sent to neurology first because they have to be seen by uh ophthalmology. The problem with acute uh ophthalmology service is that they don't provide on call uh in at least in small hospitals. So the eye casualty, for example, in Kings May Hospital is in uh Chesterfield Royal Hospital. So it's not always easy to get an opinion from an ophthalmologist if somebody loses their sight uh in at weekends or in the evening, if the visual loss is very acute and uh last only for a few minutes. Uh quite often it's caused by central retinal artery occlusion, retinal detachment or a vitreous hemorrhage. Uh certainly quite often this problems cause permanent visual loss. But if they are might, they may cause transient visual loss, what we call amauroses, food drugs. If the symptoms uh develop over hours, uh not very abruptly, quite often. It's caused by other conditions like uh anterior ischemic optic neuropathy, uh acute uh glaucoma. Some people have visual loss uh when the symptoms reach a plateau over days or weeks. This can be optic neuritis or uh uh macular degeneration and people who have chronic visual loss uh on one eye. Uh It can be caused by glaucoma, dry macular degeneration, diabetic retinopathy or even cataracts. Just one condition that we cannot miss is temporal arthritis, which usually affects people above the age of 50 with a new onset headaches, cough tenderness, uh jaw claudication, transient visual loss, weight loss, polymyalgia, rheumatic symptoms. This is a form of vasculitis. Uh If we have a high index of suspicion, we can start treatment with steroids uh without getting the definite diagnosis. Uh blood test showing raised ESR and CRP are a are a prerequisite for the diagnosis. But uh we like to confirm it with other tests like uh trans uh temporal artery Doppler study or Mr angiography with specific uh vas uh vascular or uh vasculitis sequences and the temporal artery biopsy. Uh probably I would skip motor neurone disease. Uh Let's just talk uh two minutes about epileptic seizures. So we all know that in the last few years, the classification of epileptic seizures changed a little bit. Uh They like to use these new terms, focal aware seizures, focal impaired awareness, seizures and focal to bilateral Tony clonic seizures, but it doesn't really change uh in clinical practice. So people either have focused seizures or generalized seizures. The most common generalized seizures are absences or tonic clonic seizures. There are some epilepsy syndromes that we have to recognize uh like childhood absence, epilepsy, juvenile myoclonic epilepsy, some rare uh conditions where specific treatment is available. We have this young girl in uh in her first pregnancy who has a history of childhood absence epilepsy. A year ago, she had a convulsive seizure after a night out with friends, but she didn't seek medical attention at the time because she felt it was down to using some drugs. Uh She's referred following a second convulsive seizure and uh she told me about upper body jerks first thing in the morning. How would you manage her seizure disorder? Would you be concerned to use epilepsy drugs because she's pregnant. Uh Would you start her on carBAMazepine? So the inva levetiracetam or prescribe bucca midazolam in case she has another conversive seizure. So, in my opinion, the best and the only option from this list is the use of levetiracetam. Uh people who present with convulsive seizures and there is a chance of a syndromic diagnosis uh because this lady had a lifelong predisposal predisposition for seizures. And also she has mourning myoclonic jerks which raise the possibility of juvenile myoclonic epilepsy. Uh not giving her epilepsy medications in pregnancy is putting her life at risk because uh pregnancy, especially giving birth and the postpartum period will increase her risk of trigger seizures from tiredness or, or sleep deprivation. And uh not giving her epilepsy medications would, would put her at higher risk of having severe seizures. So we have to choose a medication that is safe to use in pregnancy. CarBAMazepine has a relatively good safety profile. But the problem is that uh carBAMazepine is a sodium channel blocker that helps mainly focal epileptic seizures and also convulsive seizures. But it can uh aggravate uh myoclonic jerks. So, in this condition, uh in in this case, carBAMazepine is a no, no sodium val is a very effective epilepsy medication. But uh in recent years, uh there has been more and more evidence of severe teratogenicity and uh uh affecting uh the outcome of pregnancy. So it's, it's uh absolutely contraindicated in pregnancy as a first uh uh line medication starting levetiracetam would be the best option for her because Levetiracetam is a drug that can help and generalized seizures and can also help myoclonic drugs. And it has a good safety profile in pregnancy. Bco midazolam is a very effective drug to help as a rescue medication, convulsive seizures, but it doesn't prevent seizures. So it would not be the best option for her. So, generally speaking, anti seizure medications uh uh for generalized seizures, uh the best options are sodium v lamoTRIgine, levetiracetam, topiramate in absence seizures, etosuximide, um sodium v and topiramate are teratogenic. So, the risk of teratogenicity is fairly high. And in the case of sodium V, there is good evidence that uh Children who are exposed to sodium vap in the womb are at higher risk of developing autism, lower IQ. And uh there is an interesting finding that also men taking sodium vop uh uh their Children are at also higher risk of having uh autism or other neurodevelopmental disorders. So, um sodium val and also topiramate, which has uh higher teratogenicity. Uh patients who are at risk of getting pregnant need to be enrolled in a pregnancy prevention program. And they can only use these medications in pregnancy if uh they exhausted any other options and they have severe epilepsy. Generally speaking, uh lamoTRIgine and levetiracetam are safe to use in pregnancy. So these are the medications of choice for focus seizures. We usually use either levetiracetam or sodium channel blockers like lamoTRIgine and carBAMazepine. As I mentioned, lamoTRIgine and levetiracetam are the first uh choices in pregnancy. I just like to finish my talk with 22 more slides. So for women in child bearing age, uh we have to always consider uh the risk of teratogenicity or poor outcome of pregnancy. I mentioned that sodium rate and topiramate are absolutely contraindicated in pregnancy. Uh These medications are also used in migraine and uh uh they are definitely not used in migraine if there is any chance uh women can fall pregnant and only in uh severe epilepsies where other medications don't work. Uh they can be used uh antithrombotic drugs in pregnancy. Definitely, warfarin cannot be used. Clopidogrel cannot be used. Uh Aspirin and low molecular weight heparin are the choices. Immune suppression is unfortunately used in many women with pregnant because autoimmune disease is more common in younger people. Uh azaTHIOprine is a choice that can be used. Mycophenolate, for example, is contraindicated and uh steroids can be used if there is a strong indication, migraine is the most common neurological disorder that we see in the neurology service. And uh um we can use if someone has high frequency migraines uh uh during pregnancy, a low dose of propranolol amitriptyline and the paracetamol ibuprofen aspirin can be used for migraine attacks. There is also good evidence that Triptans are safe to use in pregnancy. And uh the last uh thing I just like to mention that uh many people with neurological conditions have uh have uh uh issues with driving. So the D VRA sets strict regulations for driving bans uh with certain neurological problems. For example, following ati or stroke, uh uh people cannot drive for four weeks in stroke, uh victims, they have to fully recover from all the neurological symptoms uh or have uh no limitation in limb movements and visual afield before they can go back to driving after four weeks following an isolated epileptic seizure. If we don't find an identity, a treatable cause like a tumor or, or we don't make a diagnosis of a, a generalized epileptic seizure disorder. They can go back to driving after six months. People who have an established diagnosis of epilepsy, they can drive only if they are seizure free for 12 months and compliant with the treatment. People following a simple faint, if uh they meet the usual criteria of a faint, like there has to be prodromal symptoms, there has to be some positional elements like uh getting up or being up uh when the symptoms start and some provocation factor like uh pain or uh or uh medical procedures, they usually can go back to driving straight away. Um People who have benign tumors like uh a meningioma, they can drive if it's an incident, uh finding and not requiring any treatment. People who have malignant brain tumors with high risk of causing seizures or neurological problems. Uh They cannot drive at least for two years when treated and they, they cannot return to driving. Uh If there is no treatment available, many people with neurodegenerative conditions like Parkinson's disease or dementia can drive if the symptoms are well controlled and there is no significant cognitive impairment or no significant daytime sleepiness. Ok. I'm, I hope the talk was not too exhausting to you because I know I know it was a lot, but II thought that uh that would be my, my way to help you preparing for your exams. Um Thank you so much. Doctor Sabo. It was brilliant. You covered so many topics. Thank you so much. Yes, sir. II hope it was helping you to understand the, the variety of what neurology covers because certainly I had to touch on many, many subjects. So I thought it was definitely very helpful because the neurology is one of the difficult topics. And I'm sorry. So it was a very good talk. Is there anything uh you want to ask or anybody? Um Thank you in the chat. Um No questions at the moment. Ok. If if you have any neurology specific questions and you, you, you don't know what is the best way for example, to a question in a question? Thank you. I'm I'm very happy to be contacted. So Marie knows my contact details so you can, you can make it public and uh anybody can contact me if you have any specific questions regarding neurologic questions. Sure. So if you have any questions, please do pop it down and we'll send an email to Doctor Sabo and he's very happy to help us out. Thank you so much again, Doctor Sabo. Ok. Thank you very much. Bye bye. Thank you very much. Bye time for questions. Um If you do have any questions from that talk, um or just any questions in general, just put them in the chat and then we'll look at them later in the day or we'll try to address them. Um Otherwise for now, we will um to have for lunch. Uh We'll put a feedback form in as soon as we can. All right. Thank you.