Neuro | The Neurological Exam | Dr.Eman Hassan

Indexed: 2026-05-21

[00:00:09]Dear students, this lecture is not designed for you to study neurological exams in depth or to fully understand them. It's simply a summary of neurological exams for the final exam, so you don't need to study extra details or information that won't be helpful.

[00:00:30]Students who want to delve deeper into this field in future years can refer to McLeod's book or study the original lecture, not this summary.

[00:00:43]When discussing neurological exams, we start with the evaluation of level consciousness and the assessment of consciousness level. Level consciousness is usually assessed through the glaucoma scale. The glaucoma scale is extremely important, so focus on it for the final and memorize it like your own name.

[00:00:59]We typically evaluate the eye opening out of four points, the verbal response out of five, and the functional response out of six.

[00:01:07]The total is 15. The minimum class score a patient can receive is three. For example, if they receive one point for no response in the eye, one point for no response in the verbal response, and one point for motor response. Regarding the eye response, if the patient opens their eyes on their own, they receive four points. If they only open them to speech, they receive three points. If they only open them to be heard verbally, they receive two points. If there is no response at all, they receive one point. For the verbal response, if the patient is oriented, alert, and responds and speaks with us, they receive five points. If they are confused and slightly disoriented, they receive four points. If they produce a word ( not a sentence), they receive three points. If they produce only inappropriate sounds (voices), they receive two points. If there is no verbal response, they receive one point. Regarding the motor response, if they have commands, they receive six points. If they can localize the pins, they receive five points. If they can draw a rope to pins, they receive four points. If there is abnormal flexion to pins, they receive one point. Three extensions, two of which I'll take, and one non-response. I'll go back and focus on the glass colitis skill; it's very important, memorize it for the final speech exams.

[00:02:13]Usually, I have the patient speak normally to see the volume of speech, rhythm, and clarification. We might give them a freeze to see if they produce sounds through the thong, twist, or lips, and see if they can produce them. We might have them count from one to 30 or from 30 to one to see the vitiability, which helps us assess neuromuscular disorders. We might have the patient cough or say "ah" to see the softness in the triazine. Speech abnormalities are very important, focus on them and study them well. First, we have dysarthria, which is a problem with articulation of speech, and this is usually seen in bulging, pseudobulbar, sciatica, myasthenia gravis, and Parkinsonism. We also have dysphonia, and we have loss of speech.

[00:02:54]Volume loss is a result of dysgraphia. We have dysgraphia, which manifests as a disruption in speech production. It causes abnormalities in speech production and understanding, and may also affect writing and reading. The most important aspect of dysgraphia is assimilation. How do we examine it?

[00:03:09]Have the patient speak normally. We observe the fluency and content of speech. We can give them objects to name, for example, "This is a hundred," "This is a piece of paper." We can give them a simple repetition command to see the coherence between commands, because it's important not only for coherence between speech but also for speech. We can have them point with their right forefinger to their nose, then point to their left forefinger, then point to their left forefinger, and so on. We ask them to repeat simple sentences to see the repetition to determine if we have a conductive dysgraphia. We want to see if they have the ability to read newspapers or write, and we look at their handwriting.

[00:03:47]Okay, the language difficulties that occur are very important, so you need to focus on them and study them well for the exam. The first one is expressive difficulties, which occur in the prox area or motor center. There's usually a problem with production and fluency of speech, and often even repetition is affected. Receptive difficulties are sensory difficulties; the problem is with compression, and this usually occurs in phonics. Conjunction difficulties cause a problem with repetition; they can repeat sentences if given a sentence. This usually occurs in orthography.

[00:04:29]Global difficulties occur in all speech, whether it's compression or full articulation. There's a problem with reading comprehension, meaning writing. Numbers and function difficulties usually occur in all speech, whether frontal, oxy-ventral, or temporal. The periaretal has main functions, and even the periaretal and temporal have dominant and non-dominant sides.

[00:05:01]Each one has a non-dominant side, meaning functions and legs.

[00:05:08]Disruption can occur as a result of this cortical function.

[00:05:10]These two slides are about the cortical function; focus on them for the final exam. It's very important that you know each area and what things the stasis in the gate is responsible for. Usually, the first thing we do to check the stasis is to have the patient stand and place both legs next to each other. If they are unbalanced with their eyes open, we consider it spherical abnormality, meaning two-to-spherical ataxia.

[00:05:34]If they are unbalanced with their eyes closed, we consider it sensory ataxia. If they have full tension, but they close their eyes, place both legs next to each other, and stand, we consider it a positive rumble test.

[00:05:44]If they have full tension, and this we see in the sensory ataxia gate, we have the patient He walks normally, and we look at his gait. We might find, for example, Parkinson's gait, which is seen in the stumps and small steps. We might find spasmodic gait, which is usually seen with a motor neuron disease. We might find stroke-like gait, which causes hempelgic gait. We might find Trendelenburg gait, which is seen with proximal muscle movements. We might find high- stepping gait, which we see in people with foot drop. After looking at the normal gait, we ask the patient to walk in the tandem gait, which is one leg in front of the other, or to walk on tiptoes or on a walking stick. This table shows all the abnormal gaits, meaning the gait disorder order and what the main diseases are that cause this abnormality. So this table is important; you must memorize it. Then we move on to movement in general so that we can perform complex and coordinated movements.

[00:06:47]More than one part of the nervous system works. We have cortical centers or high centers, motor neurons, and so on. We have input coming from the brainstem, and the exciter from the subcutaneous system. We also have sensory pathways that help with transmission and assist in joint positioning. Now, when examining the motor system, we start with the inspection, then we check tone, power, and relaxation. Finally, we check the coordination. If we want to examine the neck and trunk, I always check the static induction first. I check the static induction first, then I start examining the motor system. If we start with the inspection, the first thing we look for is the muscle tone. If we have muscle hypertrophy or muscle wasting, you know, we usually see muscle hypertrophy in people who do bodybuilding, but it can also occur in psoriasis, where the muscle tone is visible. It's large, but actually weak. I see it in people who have muscle dystrophy. We might have muscle wasting in the lower motor neuron disease, and it's usually more pronounced than primary muscle dystrophy. So, when we have primary muscle disease, when myopathy works on muscle wasting, it's not like the wasting caused by irritants, which is neurogenic wasting. Usually, the loss of muscle with neurogenic disease is much more noticeable. Yes, upper motor neuron disease or leggings, if they persist for a long time and we have muscle wasting, can cause muscle wasting and atrophy. So, muscle wasting is usually a sign of lower motor neuron disease, but also, prominent upper motor neuron disease or leggings can cause muscle wasting and atrophy with muscle wasting. Now, usually, to determine neurogenic wasting, we need to determine if the combination in The lower motor neuron has become a duodenum to aneurysm, horn cell disease, spinal cord, or palpable nerve. For example, when a patient has wasps or flukes in the intracranial cells of the hand, I look at these wasps. If they are venous, even though the small hand cells are normal and responsive, then I say that the problem is in the medial nerve, which is carpal tunnel syndrome. But if there are wasps in the small hand cells, then the problem is in the nerve. And if everything is normal and responsive, then it means we have at least one level of cerebral vascular disease or aneurysm. Now, after we look at the cells, if we have wasps or hypertrophy, we look for abnormal movements. We explained abnormal movements to you in the Movement Disorders lecture, like the term, the chorea, the athetosis, and the dystonia, so I won't repeat them. I removed them from this lecture, these slides, and this recording because we explained them to you in detail in the Movement Disorders lecture, so there's no need to study them again. However, as I said, if anyone wants to study this lecture in depth for the physical exam, this lecture is only for exam purposes.

[00:10:00]Fasciations are abnormal movements that we didn't discuss in the Movement Disorders lecture. They are a touch that occurs, like a skin twitch, and this usually happens in the lower back, especially in patients. You'll find they have a twitch, and you'll find they have a movement. Of course, the patient doesn't feel it, but we see it. Even if we perform a stimuli on the muscle itself, we'll find the fasciitis appears directly. We have physiological fasciitis, which we see in the calves, meaning muscles, and we have myoclonic fasciitis, which is not pathological. It's when the patient has involuntary movements. This is how patients feel; they experience eyelid twitching or first-person intraocular twitching.

[00:10:54]This is usually not pathological and occurs with irritability, stress, or lack of sleep. We, in pathological vasculature, talk about these in restin muscles. The patient doesn't feel them, but we see these twitches, or on EMG we find fibrillations in the muscles themselves. This is usually due to diastasis recti, so it's a myoclonic syndrome. We talked about it in our lectures. We talked about it in the episiotomy lecture. It's a connection that occurs in the occipital muscle. It could be vagus, conus, synovial, or it can be divided according to the anatomy or level responsible for it. It could be a diastasis recti, a brain dam urticaria.

[00:11:46]And don't forget that we have physiological gyri that occur when someone is about to fall asleep; they feel a twitch in the carpal muscles. We call this a hypnic gyri. Physiological movements aren't scary; we're talking about pathological ones. A patient with myocardial incontinence might tell you, "I have tremors in the morning when I first wake up." We call this myocardial incontinence. We see it in myocardial incontinence. Or you might be examining a patient in the clinic with Parkinson's disease and you find sudden, shock-like movements in their hand or leg. These are what we're concerned about; they're pathological. Other abnormal movements, which we see during inspection, I won't go into now because we explained them in detail in the Movement Disorders section. Now, after discussing inspection for abnormal movements, we'll talk about assessing tone.

[00:12:30]Tone is the resistance of the joint when we move it passively. Usually, before we start moving the joint passively, we have to ask the patient if there's any discomfort in the movement. Then we start moving the passive latch joint with a full range of motion, sometimes slowly, sometimes quickly, to see if we have redundancy or spacing in the pulsating direction. Usually, it's contagious, meaning don't let the patient move with you; move on your own without the patient moving so you can feel the tone and assess it correctly. Usually, when we're assessing tone, we either have hypotonia or hypertonia. This means the normal human tone [clears throat].

[00:13:14]Normal tone has a minimum resistance to movement, but it's not very strong, nor is it very weak, meaning you can move their hand freely without them resisting at all. So, normal tone usually has a minimum resistance to movement. If the resistance is completely gone, that's hypotonia, and if the resistance is very strong, that's hypertonia. This is the main abnormal tone that It occurs during tone assessment. Hypotonia is usually seen with muscle spasms and hyperlexia in lower motor neuron diseases, and it can also occur in erysipelas or spine shock. Hypertonia is usually seen in lower motor neuron tests if it is [ __ ], and if it is rigid, it is seen in extramed. Extramed, if it is normal, shows spasticity; if it is extramed, shows extramed rigor, like Parkinson's disease. These are all extramed. Spasticity means increased resistance, and we are examining tone, which is the resistance that increases with velocity and rapid movements. For example, in mild cases, you might find a catch occurring when you move during passive movements, either at the beginning or end. In spherical cases, you might find a contraction, meaning a limitation of the range of movement, along with a contraction present in the patient.

[00:14:32]Hypertonia is found in the upper limbs, specifically in extension and flexion. In lower limbs, it's called spasticity or hypertonia, which is described as [ __ ].

[00:14:41]We see it more often in the upper limbs. In flexion, there's a resistance, but this is outside the extension. Reduction isn't related to speed, unlike in the lower limbs. Usually, if it's across the entire range of motion, I call it lead pipe redundancy. If it's a start-stop result of the trimmer, meaning there's an interruption between the movement and the trimmer, I call it cochlear flexion. It's a sign of extrapyramidal spasticity. For pyramidal flexion, if it's across the entire range of motion, it's a lead pipe. If it's a start-stop with a trimmer, I call it cochlear flexion. Closure is a series of connections that can be two-fold, which is logical. This is less than six beats in a row, which is physiological. We're more than six beats here. We're talking about upper motor neuron disease, which is a sign of upper motor neuron disease. It's very important. You should know that the clones are present when we stretch the muscle or the tendon. After we finish the tone test, we go to the power test. Of course, the power test is the same.

[00:16:01]We ask the patient if there's any movement or mobilization. We have them raise their hands as if praying. We try to get them to close their eyes for 30 seconds and see if there's a protractor drift. This is also a sign of upper motor neuron disease.

[00:16:15]After that, we start to see if there's an overgrowth of gravity. If they move their hand, they raise it. If there's an overgrowth of gravity, or if they move a jar, they raise it.

[00:16:22]Then we start to put resistance to the movement because of the stress on the single joint protractor drift. Usually, I have the patient perform arm stretches during the subduction phase. The palms are up, almost as if praying, with their eyes closed. We count to 30 to see if there are any pyramidal woes. If the affected side is alone, the hand will perform bronchation and drift. This is an early feature of the upper motor neuron ligand. So, if we want to look for upper motor neuron disorders, we need to look for clones, hyperflexia, spasm, and bronchial drift. You need to memorize these signs, which we see in the upper and lower motors. They are very important for the final exam.

[00:17:11]Tranquil strains: I try to look at the proximal muscle and truncal strains to see if there are any truncal woes. So, I have the patient sit in a chair, fold their arms, and try to stand up and sit down. Without using his hands to see if we have any twists, we then proceed to examine the power agent resistance. We apply resistance and examine each movement or muscle individually. So, we examine shoulder abduction, hip flexion, hip extension, rest flexion, rest extension, finger flexion, finger extension, and thumb abduction. Of course, each movement has a muscle, nerve, and nerve root. This table is essential to memorize; don't go into the exam without memorizing the upper and lower limb tables, whether for movement, muscle, or nerve stimulation. I will go through these tables because they are strictly memorized, and it's crucial to memorize them. They are very important for the final exam.

[00:18:26]This image illustrates the movements: for example, hip flexion, hip extension, which nerves are responsible for it; similarly, ni flexion, ni extension; dorsal flexion, dorsal extension; ankle dorsal flexion; and all plant reflexion or extension. It's explained in the previous table, so if you've memorized the table, you can skip over it. Now, how to scale muscle power? You know, we have MRC scales from zero to five.

[00:18:57]Normal power is five, movement against resistance is four, movement against resistance is three, kinetic energy is two, flaccidity (meaning no contraction without movement) is one, and there's no muscle contraction, so it's zero. You've used this table a lot in assignments, so you've probably memorized it, but just skim over it. Read it, understand it, don't memorize its definition or details, just know it. You also need to know the finishing principles. It's important that the parameters we have are: parasitology, plegia, capillaries, mongia, singia, and dermal. Now, the wickets are: if it's without a group, it's a motor neuron; if it's a phenotype, it's a lower motor. Neuron, and don't forget the hoversigne. When a patient comes in and says, for example, that they have a weak on one side, I tell them, "Okay, raise the other side." When they raise the other side, the side they say has a weak and can't move at all, if it's not actually a weak, we'll find that it has a hip extension. So we have the heel of the patient, meaning you can feel it in the lower right heel if you put your hand under the patient's heel. This hoversigne helps us decide if the patient is functional or if they have true weaknesses. In general, if there's a large group of affected muscle, it's a high-end lumbago motor neuron. If there's an individual affected muscle or individual nerve, it's a lower lumbago motor neuron.

[00:20:34]This page or slide is very important when we have weaknesses in the wrist and finger extensions. We see if we have several weaknesses and if there's precancerous squamous contracture or not. We have spirochete wicks and pericardial involutions.

[00:20:49]Most ligation is in the radial nerve. We also have mild wicks and pericardial involutions. " Not cut here" means C.S. root ligation.

[00:21:01]If we have wicks in the ankle, the flexion inversion indicates foot drop, while the ankle inversion indicates common junctional ligation.

[00:21:12]However, if we have rotation and inversion, the root ligation is in the ankle.

[00:21:22]This page is very important, and this slide is very important, so study it and memorize it well.

[00:21:28]Primary muscle diseases usually have proximal wicks, while motor polyneuropathic diseases cause dilated wicks.

[00:21:35]Upper motor neuron diseases usually cause pyramidal wicks. We find more wicks in the extensors than in the flexors in the upper limbs, and more flexors than extensors in the lower limbs. So, to summarize what... The things we learned about in the motor neuron, we talked about closing, we talked about spasticity, we talked about restlessness, we talked about the pyramidal distribution of flexors. We find flexors more often in the extensions, in the upper limb, and more often in the lower limb. I mean, I'm looking at this. Try to do a habit to get this reflex. We have sensory and anterior motor neuron flexors between the monosacral reflexes. Now, how do we get the reflex? This isn't important for the final exam. You'll understand more later by reading more on the subject. But usually, the reflex is an involute contraction of the response to stretch. Now, how do we test it? The patient is usually in a relaxed spinal position, but sometimes exposed. I mean, the upper limbs need to be tested with the patient sitting, but the lower limb needs to be lying down, or if they are lying down, they should be lying on the edge of the bed to make them comfortable. To properly visualize the reflex, the patient must be relaxed and comfortable, and there should be no pain or discomfort. Pain or discomfort usually causes the patient to develop hyperlexia. It's very important to feel the tension before applying pressure. We're not targeting the muscle or the bone; we're targeting the tension.

[00:23:34]Look at the symmetry of the response and the reflex in the different areas. Now, regarding reinforcement, we only need it if the reflex is present. That's why students often ask me during rounds to have the patient perform reinforcement. I tell them that if we see the reflex, there's no need for reinforcement. We only perform reinforcement when the reflex isn't clear enough to make it more distinct. We need to be certain whether there's reinforcement between the patient and the reflexes to determine if it's hyperlexia. So, how do we usually... Reforcement occurs while we are examining the upper limb. It makes the patient either not perform a flexion or perform a hand fist. If we examine the lumen, it makes the patient perform interleukin-2 finger and toe hand flexion.

[00:24:20]Now, every relaxation must be memorized. We are examining it and its nerve root. This table is for memorization and is very important for the final exam. The upper motor neuron usually causes either hyperreflexia or normal relaxation. Now, we usually perform a reflex test and either say we have hyperreflexia, normal relaxation, or hyperflexia. Sometimes, if we don't have relaxation even with forcement, we might say we have eryflexia. The grade is usually plus, so we consider it hyperflexia. Closing plus, pressure relaxation plus, normal relaxation plus 1, which means hyperflexia. It may appear with forcement, and the absence takes zero.

[00:25:12]Hyperflexia is the sign of the upper motor neuron. The blood pressure Absencetics are lower motor neuron ligands. Patients with hypothalamus will experience deceleration in the limb relaxes. Patients with serpentine disorders will experience pendulum reflexes. So, when we tap on the leg, it goes and comes back more than once, like a pendulum. It might not even be present, and that's normal. Now, here's the slide; I want to explain it a bit because I feel it's not formulated clearly enough for the student. The idea is that when we have C5 or C6 (C5 and C6 spinal cord level ligands), we have mixed relaxes found. For example, when we have cord ligands at level C5, if we test the biceps relaxes, we find deceleration or absence because we have locked lower motor neuron ligands at this level (C5). If we then test the precordial relaxes, we find... It's either dimension or absence, and it might be inverted. What does inverted mean? It means that when you tap the tendon itself, the precordial, to get the reflex, instead of the flexion that usually occurs, there's finger flexion. This is called an inverted spinnet reflex. Instead of the flexion being visible, it's visible in the fingers.

[00:26:45]If we examine the triceps reflex, we find it agitated or precipitated because there's a loss of upper motor neurons above the level of C5C. If we examine extreme relaxations, like the patella (the nevi), we also find it hyperactive due to the upper motor neurons being damaged above the level. Usually, spinal cord compression occurs at C5C, causing a complex relaxation that leads to hyperreflexia in the biceps and precordials, and possibly the precordials.

[00:27:22]Inverted spinner reflexes cause finger flexion instead of bony flexion, while trajectory reflexes and lower extrema reflexes are found in the reverse.

[00:27:34]Now we want to talk a little about response. Response is when you try to move it, and you usually find a directional flexion.

[00:27:55]As for the fan, this is when we do this, meaning we move it backwards, and we find that we have a rotation in the pectoral or lower extrema, and usually... We are focusing on the Pecto and Hi- Sign Acupuncture Motor Neuron Legion, which we call it Extension Plant Response, which means Extension Plant Response Hi-Sign, while the Alpha, we call it Signoron, so you also want to add it to the Synoron, it works, but it does not work, and keep it well for the fine exam. Examine it. We will try to get it. We will try to walk it as shown in the picture. It is ok, and it is usually necessary.

[00:28:57]Contraction occurs in the underline muscle, and the amplicons move in the direction, meaning laterally up or down, in the direction of the quadrant, between sixteen and sixteen.

[00:29:10]Contraction or the underline absolute muscle. This is usually normal and will be present if there is a loss of this sign of the needle of the neuron leg. It is usually possible to be early sign as well. It is also very important to add this sign to the needles of the motor and run sign. It will happen in They have a means of los domain, real-time responses, possible They can also be lost, not just in the motor neurons. They can be lost after abdominal surgeries, or due to repetitive strain injuries, or in patients with many lesions.

[00:29:41]Now we've finished the motor system, meaning we've covered inspection, tone, power, and relaxation. But coordination is considered part of the motor system, so we usually check coordination after checking tone and power. Coordination is usually responsible for complex movement, and this complex movement should be smooth. We usually need to have specific motor function indicator sensors for this complex movement to occur. When we talk about the sulcus, the midline structures, such as the perimeter, are responsible for the body, i.e., the axis. The hemispheres in the sulcus are responsible for apse-lateral coordination. What test do we use to check coordination? We have finger noses, which are the tone; rapid tensor movements; and rebound.

[00:30:32]Don't forget to also check the stages of head nodule and tandem gating.

[00:30:37]All these things are important in the seriple exam.

[00:30:40]When we start with finger nosing, we can have the patient put their finger to their nose and then touch our finger. The distance between me and the patient must be a full arm extension. I try to move my finger when the patient's finger moves from their nose so that it doesn't affect the examination. What are the abnormalities I look for? I check if we have dystonia or past-pointing. I check if the patient is doing undershots or overshots. I check if there is intensity. When they get close to the object, they have a trim, which I call near-object.

[00:31:06]We check if the movement is slow, diffuse joint or clunky, which is dysnergia.

[00:31:12]Rapid tensor movements are usually performed by holding one hand still and then using the other hand... We perform a movement technique where we tap the palm once, then the other side, then the palmar surface, then the radius, quickly, trying to see the eye. This is called "movement." We have a problem with the movement because it might be slow and the patient's arms might be out of position. We try to apply pressure to the patient's arms downwards and the arm. If the arm returns to its original position after applying downward pressure, it's normal. But if we perform control movements that move above the original position, we call it " rebound positive." This is a sign of severe heel dystonia. Heel tone is the same principle as finger nose in abnormality.

[00:32:09]Abnormality includes dystonia, dysnergia, and tension, but the idea is to have the patient place their heel on their knee and pull it downwards or move it downwards towards the ankle, then raise it back up and place it on their knee, and then lower it back down towards the ankle, and so on. The patient will make two slides, an up-and-down motion between the ankle and the wrist, meaning between the wrist and ankle. They will try to make two slides for the heel, up-and-down motion. This is roughly in coordination with the lower limb, and usually, abnormal findings resemble finger nostril movement.

[00:32:44]We measure whether the patient is moving in a straight line between the wrist and ankle.

[00:32:49]You need to know something: to check heel tone or finger nostril movement, the patient must not have any flexion or flexion. I can't examine a patient with a sclerotherapy sign if they can move their hand or leg, because they wo n't be able to make finger nostril movements or heel tone. This isn't because coordination is affected, but because they already have flexion. The neck flexion is usually checked to see the power of the neck.

[00:33:14]If it's present, we can check for neck flexion extension.

[00:33:17]The number of flexions is very important in many cases. I usually ask about it in the proximab, and we ask about it to see if we have it. It's usually a serotonin syndrome, so we're usually interested in the trochanteric flexion flexion to see the proximal flexion flexion and to see if we have trochanteric ectasia. This table differentiates between upper motor neuron and lower motor neuron science. You should memorize this like your own name; it's very important for the final exam. This is the slide, and the slide after it. Now we'll go to the sensory model. Of course, the sensory exam has no value in examining it if the patient doesn't complain of sensory symptoms because the sensory exam is controlled by the patient, not by the examiner. This means the patient might not feel anything but tell you they feel something, and the patient might feel something but tell you they don't. So you can't judge them. If you're judging the patient on the sensory exam, then usually the sensory exam You leave it for last, meaning even when you're examining a patient in real life, you leave it for last because the information you'll get from them won't help you judge the patient. And usually, as I told you, it's controlled by the patient, meaning it's difficult to assess it 100% accurately. So usually, if the patient doesn't have sensory manifestations, there's no need to examine them. What models do we examine? Light touch, special touch, vibrations. These usually become transmitted via the flexor, and their booster column usually remains lateral to the point of entry. Between the two, temperature sensory sensors usually transmit via small slow conduction.

[00:35:19]Vibrators of the flexor and spinothalmic tracts.

[00:35:29]These temperature vibrators usually cross the contraction in the middle of the aftercourt, and all these sensory... For the sensory center, which is the periapical loop, what symptoms might we observe in the patient? As a sensory manifest, they might tell you they have parasitism, hypositism, hypersitism, or hypergesia. Each one has a specific meaning, which you need to understand through this table. Now, we examine them using the light touch. It's not necessary for the patient to close their eyes. Even when I was examining patients with you, you told me to have the patient close their eyes. I'm telling you, it's not necessary for them to close their eyes. It's enough if they look away. So, the patient will either close their eyes or look away. You try to hold it like a cotton swab and try to move it, meaning you feel it first near the patient's sternum, then try to move it with the frontal area on the dermatum. When the patient feels it, they say "yes."

[00:36:20]Of course, this means examining both sides together to compare right and left to see if there is any symmetry in the superficial sensation. We do the same thing: we tell the patient to look away or The patient closes their eyes, and we first feel the neurological pain on the sternum. Then we try to take it with a frontal area on the dermatum to see if the patient feels it. If they reach a certain area, for example, they start to feel it; if they didn't feel it before, we keep moving upwards and upwards until we reach a specific point. We circle around this point to capture the full range of sensations the patient feels and compare them. Above and below this level, we usually use cold and hot tubes, but these are n't always available. For vibration, we use a 128 Hz ten fork.

[00:37:06]The patient first feels it on the sternum, then we hold it and place it on the tip of the great artery. We ask the patient if they feel it. We can then have them close their eyes and stop the vibration to see if they say it stopped.

[00:37:20]Of course, if the patient doesn't feel it when placed on the tip of the great artery, we start moving upwards. We move upwards to the intervertebral joint, then the medial mucosa, then the tibial tuboscete, then the anterior intervertebral point. If the patient can't locate it, we move proximal to the proximal intervertebral joint, then to the metacarpopharynal, then to the wrist, then to the elbow, then to the shoulder, and so on. For probing, we usually have the patient with their eyes open, holding the gritometer and moving it up and down. We ask them, " Where did I move it? Which way did I move it?" Then we have them close their eyes and repeat the process to see if they can move something very minimally, just a few millimeters. We see if they can say they moved the finger up or down. Sensory modulation usually consists of neural nerves, root canals, spinal cords, and intracranial branches. These can then move upwards to the brainstem, then to the thalamus, then... For the bright area, nerves, and roots, these are usually disease effects. Preferred nerves cause preferred neuropathy or polyps, and the number of preferred neuropathies is in the lower extremities, meaning in the lower limbs. This is called a lentiform pattern, meaning this lentiform pattern, for example, is always present in the lower limbs, or the lentiform pattern is independent of the lentiform pattern.

[00:38:39]If sensory symptoms and findings are found in the upper limbs before the lower limbs, then we are talking about a permanent disease rather than an acute preferred neuropathy disease, or we have a problem with the spinal cord. Usually, spinal cord problems, such as disc herniation or cord ligatures, cause two types of preferred neuropathy and not acute. Loss of perception, which is pseudoathetosis, is a very important test. You have the patient close their eyes and hold their hands out, stretch their arms, and observe.

[00:39:10]If the fingers move in any strange ways, like athetosis, we call it pseudoathetosis. It's a result of loss of proprioception due to defects in the posterior column, or sensory pathway.

[00:39:19]Loss of proprioception usually occurs when the patient extends their hand and closes their eyes; we see involuntary movements of the fingers and hand resembling athetosis. This is called pseudoathetosis because of a defect in the sensory pathway that affects the proprioception of the spinal cord.

[00:39:38]Traumatic injuries or compression can occur due to, for example, a herniated disc or something pressing on the spinal cord. In the lower level of the condition, we have a decrease in sensation, while in the lower level, we have hyperstimulation syndrome. There are spinal cord syndromes and brown cortex syndromes, where loss of proprioception occurs. Spinal sensation and motor function, and the lateral motor function, are affected, while in Brown Score syndrome, we have a loss of the spinal cord. Now, what's important about its characterization is that we have lateral motor flexions, resulting in a loss of vibration and joint position on the same side where the cord flexion and loss occurred. In temperature, the sensation is contralateral. This is very important, and focus on it for the exam. In Brown Score syndrome, we have a loss, while in the lateral function, it's a loss. These played a big role in the sensation, even in the lateral motor function. Usually, like the biceps and biceps, we said, for example, that they cause a loss.

[00:41:12]Now, here we started talking about usually.

[00:41:17]If you look at the hand, you'll find that the side in blue gives this, and the side in red gives the median nerve, which is the one in the color... This purple or dark blue color I see is red nerve. Now, if we're talking about medial nerves, usually we have medial nerve pain. Now, we're talking about carpal tunnel syndrome. We have wasting in the lower amniotic fluid, and we have thump absorption. This is important to know: wasting in the lower amniotic fluid and thump absorption. This is very important, focus on it. In the final exam, of course, when we examine the thump absorption, we look at the lower amniotic fluid to see if we have wasting, and we might also examine the position.

[00:42:04]Carpal tunnel syndrome is the most common type of nerve pain. It usually occurs in women. It occurs in women with hypotension or premenstrual syndrome. They feel this sensation for months or weeks. It doesn't just come out one day. Women have had the symptoms for a while, but when they increased, they came Complain, it's important to know that we also have tenderness, pain, and woes in the thump, addiction.

[00:42:38]All these things in the table are important. For example, carpal tunnel syndrome, focus on them. Anatomical nervation, anger, and pain in the intercostal fingers, finger addiction, and finger attachment. We must examine these. We check the albos to see if we have scars or trauma, and we check the nervation sensation. The radial groove nervation, we look for woes in the arm extensions and breast extensions, and in the finger extensions, we check if we have sensor overhand and if we have low triceps. This is because the triceps muscle that gives feedback is the radial nervation. So if the radial nervation causes anger, we will have low triceps, a tense reflex, and common pronator nervation. This is very important. We talked about if there is usually a fusion. We have foot drops and high- stepping KGK jet, and this usually happens due to a fusion of the fascia head as a result of a fascia head fracture. Or, in mobile patients, or when the patient performs retinoids or squats, they get foot drops due to common peripheral nerve pain. So, foot drops happen in the common peripheral nerve pain.

[00:43:43]How do we distinguish them from a condition where the pain occurs in the aneurysm? This distinguishes it from a condition where it only occurs in the aneurysm, or what is called a mitral jejunal lesion. It is very important, so focus on it. A mitral jejunal lesion is a neurogenic lateral nerve of high- purity sensory sensation. The patient feels like they have a tingling sensation or osteopathy in the lateral aspect of the brain.

[00:44:26]I think that's the end of the lecture. I focused on the important things for the exam, so as I said, this lecture... This recording is helpful for studying this year for the final exam we have in 2026. However, if you want to delve deeper later, you should refer to physical exam books or the original lecture. Thank you all very much, and good luck! Study well for the final. Don't be afraid; study with understanding, not just by reciting.

[00:44:52]Imagine scenarios of how the patients might come in and how you will be questioned about them. God willing, you will do well on Sunday and get the grades you want and more. May God grant you success, and please forgive us for any shortcomings.