Transcript for:
Understanding Sleep and Brain Disorders

hello and welcome to the review of chapter 60 of guyton hall's medical physiology textbook in this chapter we go over sleep and some disorders of brain activity if you enjoy the chapter please don't forget to give it a like and subscribe to the channel so if we had to define sleep sleep is unconsciousness in which a person can actually be aroused from that unconsciousness due to some kind of sensory or other stimuli and that is different to a coma where a coma you are also unconscious but you cannot be aroused out of that unconsciousness and then sleep itself can be further classified into two types of sleep we've got rapid eye movement sleep also known as rem sleep and slow wave sleep or non-rem sleep and this is where the brain waves are strong and of low frequency so if we talk about rem sleep first rem sleep is more of a very active sleep it's not very restful when it occurs and cycles so every 90 minutes or so you're going to go into a rem sleep where you have further dreaming you may have active bodily movements and you are more difficult to arouse out of that sleep your heart rate and respiratory rate can also become a regular with the more active type of sleep and your brain is highly active during this time so it seems like a paradoxical type of sleep where you're almost in a state where similar to when you're awake but you are actually asleep you are unconscious whereas slow wave sleep is a very restful type of sleep where you actually recover the most and you have a greater amount of slow wave sleep and this restful sleep the longer you've been awakened the tighter you are the more of the slow wave sleep you're going to have this figure 61 here just goes through how repetitive this rem sleep is so throughout the night you're going to have this rem sleep every 90 minutes or so we do have various different brain waves throughout sleep and we'll get into how we measure these brain waves and what they represent shortly in this chapter so sleep itself appears to be an active inhibitory process we've got three ways of having sleep being stimulated in the body the first of which appears to be the main one that we've already mentioned in a previous chapter due to the rough nuclei of the lower half of the ponds in the medulla and this ref nuclei they secrete serotonin both anteriorly up into the higher centers of the brain so the reticular formation and also to the thalamus hypothalamus and the limbic system and also downwards into the spinal cord as well and serotonin has an inhibitory effect which then results in a down regulation of our neural activity and help promote sleeping we have two other ways as well promoting sleeping such as the nucleus of the tractor solitarius which receives its inputs from the vagus and glossopharyngeal nerves they seem to have a role in sleep in addition to regions of the diencephalon mainly the rostral part of the hypothalamus and a diffuse nuclei of the thalamus as well so if you have lesions in these sleep promoting areas that results in a high state of wakefulness so you're actually unable to get to sleep and the longer that you are awake you appear to actually produce transmitter substances that are also trying to promote sleep so such as muramiya peptide and several other substances i've noticed as well that accumulates in your cerebrospinal fluid so that fluid that surrounds your central nervous system and the urine of animals that are awake for several days you start to collect these particles that if you actually inject straight into the central nervous system itself you will promote sleep very rapidly so the body's very good at trying to get you to go to sleep in various mechanisms and although we don't understand the sleep wakefulness cycle very well it appears to be this positive feedback initially when we wake up so your reticular formation starts to activate wakes up and excites your cerebrum and your higher nervous centers and then over time it's believed that that center just essentially fatigues so then that excitatory stimulus the reticular formation stops up positive feedback allows these other systems to start to inhibit the central nervous system and then you're able to sleep and there's also these neurons called orexin neurons that appear to also play a role they're very active when you're awaking and they stop firing when you're asleep and destruction of these neurons results in a condition called narcolepsy narcolepsy is a really bad sleep disorder where you're very sleepy during the day because you don't have these neurons which keep you awake and you may have sudden attacks of sleeping when you may be actually doing something that would normally keep you awake like talking or walking where you could just suddenly fall asleep because you don't have any input from these urex and neurons in terms of the role of sleep we know that it is very very important and we know that through disturbance of sleep so mild sleep restriction for a few days can result in a reduction in our cognitive and physical performance overall productivity and health of people as well and everyone should know that who hasn't had much sleep in a period of time you can tell that you start to slow down your brain starts to slow down you start to become less physical and sleep appears to have this restorative effect of the balances within your central nervous system that is responsible for essentially keeping your body moving awake and ready to perform daily activities if you want to dive more into the benefits of sleep and the harmful effects of not sleeping i do recommend you read a book by matthew walker who spent his life researching sleep and what happens when you don't get enough sleep even if you just get one hour less sleep a day the detrimental effects on your health are huge so i'll leave a link for that book which isn't a textbook it's just a regular book that's really easy to read i'll leave a link for that book in the description and i do highly recommend people ever read of that book for your general health and also it will help your study practices as well so this next portion really goes over the clinical aspects of sleep and brain wave disorders but first we have to really know what a brain wave is and a brain wave is recorded using an electro encephalogram and that's recorded by putting little electrodes over your head and then getting what kind of waveform is coming from your brain and most of the time it's very irregular there's no specific pattern to it and it just looks like these guys up here which is obviously quite hard to discern because you are measuring not just a single neuron but multiple neurons at one time so when you are active and there's a lot going on and there's a lot of neurons firing the brain waves become more irregular and harder to find any patterns whereas the less active you are and the less going on then it's easier to get a pattern and the waveforms become more regular so there have been four main waveforms identified alpha waves which are at the top here which is found during an awake person who's resting and isn't necessarily concentrating on anything which then turns into beta waves once you actually start to concentrate on anything the beta waves are more irregular and harder to discern and they are lower in amplitude so once again once you concentrate on something you have more neurons firing it becomes more regular lower amplitude we have theta waves which occur during emotional stresses or during disappointment and frustration but also during brain disorders as well and then delta waves here which occurs during very deep sleep when you have very little neuronal activity as you can see it becomes more regular this is also what occurs when you actually disconnect the cortex from the subcortical regions so you remove that cortex and thalamics connection so you're just getting the electrical recordings of the cortex itself so you're reducing the amount of neuronal activity resulting in a more regular brain wave and then this figure has 64 this really shows what i was trying to describe earlier how when you have less activity you have a more regular larger type of wave such as during anesthesia sleep once you actually wake up but you're relaxed then it becomes more irregular eventually once you're actually paying attention more regular still or at least shorter and then during seizures where you have aphasia and just continuous firing of neurons that becomes even more irregular and hard to discern so if we move on to seizures now a seizure is exactly that is that it is uncontrolled excessive neuronal activity which results in an inability for the brain to function normally and it can result from multiple neurological and medical conditions basically it can be defined to intracranial meaning that it's coming from a disorder and actual brain structure itself or extra-cranial because of something outside of the body influencing those neurons such as hypoglycemia just to give one example epilepsy means that there is continuous or recurrent seizures so multiple seizures means that you have epilepsy so epilepsy can also have multiple causes just depending on the causes of those seizures but you need to have multiple in order to be epileptic and quite a few people will actually have at least one just single seizure within their lifetime approximately five to ten percent will have that one seizure whereas one percent of the population have epilepsy any drugs which promotes a seizure are called electogenic meaning that they are more likely to increase the neuronal excitation and an impaired inhibition of the neuronal activity whereas anti-epileptic drugs mean meaning that you are treating or preventing an epileptic event they attenuate excitation make it less likely to occur and make inhibition a lot easier to occur so if we talk about epileptic seizures themselves we have two types focal seizures meaning that it's defined to a focal area of the cerebral hemisphere and generalized meaning that involves both hemispheres now focal seizures can also look like generalized seizures because they can spread throughout the body as shown in this figure here we can have a focal seizure that propagates to the cortex either the epilepsy or side then over to the contralateral you can have a focal seizure that then stimulates the thalamus which spreads out to the rest of the body or you can have the primary generalized seizure meaning that it just activates the entire cortex at one time if you have a focal seizure that does not spread clearly you're going to have the outward clinical signs relating to the portion of the brain that is having a seizure and you can have focal seizures from scar tissue a tumor a destroyed area of the brain or congenital derangement in the local circuitry and it's believed to mainly occur due to localized reverberating circuits you know spiraling around in one area causing a constant neuronal input in one particular area of the brain if it does result in a generalized seizure we can see something called the jacksonian march which means that there is a march of contractions of the muscles throughout the opposite side of the body usually starting in the mouth region and then going downwards towards the legs when it comes to generalized seizures all areas of the brain are stimulated simultaneously and that can result in grandma seizures which is the hollywood style seizure full body shakes or the more scientific name being generalized tonic clonic seizures and that can last for a few seconds to up to three to four minutes it can result in this post seizure depression usually with seizures you may have a preectal period or this aura meaning that people may feel a little funny they may have it jerking in certain muscle movements depending on where the seizure is about to start and there's almost a preemptive feeling of a seizure about to occur the seizure occurs which will result in excessive neuronal discharge and therefore stimulation of whichever portion that that seizure is within and then you have a post-ictal period where the region that was stimulated now no longer fires for a portion of time so if it's your entire brain then you can have this post-seizure depression where the entire nervous system just remains in stuba for a couple minutes or so now the majority of tonic-clonic seizures are idiopathic and there appears to be a heritary predisposition and they can be precipitated by several events such as emotional stimuli alkalosis from over-breathing drugs fever or loud noises and flashing lights that's what we know from hollywood as those flashing lights inducing epileptic seizures and then what actually stops a seizure it seems like there's active inhibition that occurs from the inhibitory neurons being activated from a generalized excitation that then slows everything down it stops the seizure there'll also be an element of fatigue as well of every single neuron firing at once there's also a type of seizure called the fatigue ball seizure which is really the absence of seizures it occurs in childhood or early adolescence and typically goes away by about 30 years of age and that's almost the absence of outward signs of a seizure where you have a few seconds of unconsciousness steering off into space maybe some twitching of some muscles and then a rapid return of consciousness with the resumption of the previous activities occasionally they can result in a generalized tone of climax attack when it comes to treatment it really just comes down to blocking the initiation and the spread of the seizures so there's various drugs here where you may want to block sodium channels alter calcium currents increase gaba activity on inhibitory neurotransmitter or inhibit receptors of glutamate or excitatory neurotransmitter or there's others with multiple mechanisms of action sometimes there are surgical fixes if you're able to localize exactly in the brain where the say a focal seizure is coming from now if we now get to psychosis or disorders of brain activity we've already talked about a couple but usually what the underlying causes is an abnormality in a specific neurotransmitter so for instance parkinson's disease is a deficit of dopamine release in the substantia whereas huntington's disease is a loss of the gaba secreting neurons so we'll just briefly go over these ones here we have depressive psychosis or mental depression that appears to be a diminished formation of norepinephrine which is our excitatory neurotransmitter that excites the entire upper centers of the brain or serotonin and this can result in unhappiness misery loss of appetite loss of sex drive and severe insomnia as well now norepinephrine remember comes from the locus cerealis and serotonin comes from the midline raph nuclei so the treatment at the moment for these types of psychosis or depression is actually trying to increase your norepinephrine or serotonin either through monoamine oxidase inhibitors which are meant to break down norepinephrine and serotonin or your tricyclic antidepressant such as amitriptyline which blocks the reuptake of norepinephrine and serotonin into the nerve ending so they're able to stay in that synaptic cleft for longer and continually excite the neurological tissues when it comes to bipolar the medic stage appears to be too much of neuroepinephrine and serotonin which is usually meant to give you a good sense of well-being but too much of that can cause mania so treatment includes drugs that actually diminish the formation of norepinephrine and serotonin such as lithium compounds schizophrenia which is defined as a disorder of hearing voices delusions intense fear or feelings that are unreal or high paranoia there appears to be three possible reasons for this disorder either blocked areas of the prefrontal lobes which are normally excited by glutamate neurotransmitter and the theory behind that is through lesions and monkeys and the prefrontal lobes appear to have schizophrenia-like syndromes the second possibility is excessive excitement from dopamine neurons and the reason behind that one is that parkinson's patients treated with the drug aldopa that increases dopamine they also appear to develop these types of signs similar with schizophrenia and the same for the treatment of schizophrenia involves decreasing the secretion of dopamine and then lastly here the other possible cause is abnormal function of the limbic system in the hippocampus since people with schizophrenia appear to have a smaller hippocampus what is the cause or effect and the last disease here is alzheimer's disease which is really premature aging of the brain beginning in the mid adult life that results in primarily memory loss but also the deterioration of language physiospatial deficits basically dysfunction of the brain you can no longer remember or perform normal activities and there appears to be an accumulation of this beta amyloid peptide within the brain of people with alzheimer's disease making it a metabolic degenerative disease and there also appears to be an association with some cerebral vascular disease such as hypotension or atherosclerosis and that really summarizes our chapter for today if you'd like to support the channel once again the patreon link you can find downloadable audio files it would mean a lot if you're able to support the channel otherwise i hope you enjoyed the video feel free to drop a comment and we'll see you in the next chapter