Brain Cancer Signs And Symptoms

>> today we're going tocompare motor systems. we've already discussedthe anatomy in detail, but today i want to comparethe corticospinal system, the cerebellar connections andthe basal ganglia circuitry, all of which we've described toyou previously in some detail. but today the emphasis is goingto be on the clinical signs and symptoms, showing youpatient videos that correspond to damage in any ofthese three circuits. the most important circuit,the final common path

down to the spinal cord isthe corticospinal tract. so let's start with that. the corticospinaltract takes its origin from the cerebral cortex. i'm outlining thecentral sulcus, which separates frontallobe from parietal lobe, and motor areas fromsensory areas. and the area thatgives rise to fibers in the corticospinal tractactually includes the

somatosensory cortexor postcentral gyrus. the precentral gyrus, which weassociate with motor cortex, and a wedge of premotorareas that are involved with speech and motor planning. so we have a wedge sortof like this that is going to be our origin forthe corticospinal tract. so the colors here representneurons in the precentral gyrus, the motor cortex,that are descending through the internalcapsule and a rainbow

of axons representing theleg, the body, the arm and the face areas as youmove from medial to lateral. and they are travelling down anddescending in the posterior part of the internal capsule, and then they enterthe cerebral peduncle. i have another animation,also from the university of washington digitalanatomist project, showing the internal capsule andcortex in a bluish-purple color. and you're going to see howthese fibers then descend

through the brain stem,which we're sectioning here. and the blue fibers come downthrough the midbrain, pons, medulla and cross at thelevel of the beginning of the spinal cordto the opposite side. and so each hemispherecontrols the other, or opposite, side of the body. so this is going to be importantfor you to remember that disease of the corticospinal tract above the cord manifestsitself on the opposite side.

the cerebellum is attached by its three peduncles beneaththe occipital pole and lobe and to the brain stem. and it has variousregions which we are going to show you on this specimen. this is the superior surface. so you would be looking at it if you were lookingat an mri like this. these are the hemispheresand the area

in the midline iscalled the vermis. so there is the vermisand the hemispheres, the superior surface andthe inferior surface, also with hemispheres. the vermis is a little harderto see on the inferior surface, and it's hugging the brain stem. and here you can see thetonsils that sit right over the foramen magnum. if we look at this ina mid-sagittal section,

here we have, thisis the midbrain. here is the medulla,the fourth ventricle. here is our midlinevermis of the cerebellum and the cerebellum vermisis separated into two areas. one an anterior lobe that is infront of this primary fissure that i'm opening up here. so this is the anterior lobe. we're going to come back andtalk about that when we talk about alcohol disease.

and then this is therest of the cerebellum. and on the inferior surfacenow; i turn this around. so here's the hemisphere. here is the pons with my thumbon it, here's the medulla. this little area out in herecalled the flocculus is also involved with eyemovements and balance and vestibular functionof the cerebellum. so now let's go and lookat the basal ganglia. let me remind you of some of thestructures of the basal ganglia

in this coronal section. let's get oriented. here we have the body of thecaudate, it's much smaller at this level, out here nextto the lateral ventricle. and we have a largethalamus on either side of the third ventricle. and we have a bright,white internal capsule, the posterior part ofit coming down here. and laterally out to theside we have the putamen,

which is a little bit darkerthan the globus pallidus. the pallidus has two parts,an internal and external. and the putamen is verysimilar to the caudate in its appearance in its cells. and together it iscalled the striatum. there's one otherstructure, which i can see, but it's very difficultto distinguish, called the subthalamus thatis part of the circuitry. and then finally we havethe substantia nigra that is

at the level of themidbrain that works with the basal ganglia asthe nigrostriatal pathway. i have a diagramhere that i've made to summarize thesethree circuits. so our most important circuitis the corticospinal tract, also called the pyramidal tract,which is important for willed and voluntary movements. and we're going to lookat that in more detail. we have our cerebellarcircuit which works together

with the cord andthe cerebral cortex. and we have our basalganglia circuit. so we're going to discuss eachof these in order and look at the signs and symptoms. the first one we're going to study is the corticospinaltract. so it is the chief. it is the final commonpathway that goes from the cerebral cortex down,as you saw in the animation,

crosses and decussatesat the level of the top of the spinal cord,continues down to the neurons in the spinal cord that go out to the voluntary,striated muscles. and these are called the lowermotor neurons, which are going down to the muscle endplatethrough the motor neurons. and these others are calledthe upper motor neuron. so it's a two-synapse pathwayand we have signs and symptoms that are developed when thereare damages to either the upper

or the lower motor neurons. we're going to look atexamples of increased reflexes, signs of spasticity andclonus, babinski sign, hemiplegia or hemiparesis. hemiparesis is a weakness. finger movements and finecontrol of them, and the loss of control when you damagethe lower motor neurons and get paralysis, areflexia,atrophy and fasciculations. we're going to lookat this young girl

who is being testedfor her reflexes. and this is a demonstration ofhyperreflexia on her right side because only one side of her corticospinaltract has been damaged. and he's testing nowfor ankle reflexes. but again he's going to showyou her knee jerk again. and sometimes the spreadfrom the more normal side like this one spreadsto the other side when there is severehyperreflexia.

but now watch here,it's very pronounced. and this is an excellentexample. and she also shows someother things in a moment. the babinski sign is a sign that indicates corticospinaltract damage by the large or big toe going up andthe other digits fanning. this is also called theplantar extensor reflex. but most people say thatthis is a babinski sign, and when it's present it'sa positive, meaning present,

babinski sign, another indicatorof corticospinal tract damage. this is an example of clonus. clonus is an oscillationof flexors and extensors when the achillestendon is stretched. it represents another positivesign of corticospinal tract or upper motor neuron damage. this is our young lady again, and she is beingtested for muscle tone. and the tone is extraor excessive

such that there is anincreased resistance as he moves her rightarm and her right wrist. and compare how much more limberor easy to move her left arm is. this one has resistance tovelocity and also to movement, and that is beingperformed passively. so spasticity is increasedresistance to passive stretch. and sometimes as itresists it gives way and a phenomenon calledclasped-knife is described as the feeling the physician has

as the tension changesduring this maneuver. dr. larsen is continuingto test this girl. and in many cases fingerflexors are severely involved, because that's oneof the main purposes of the corticospinal tract. a large number of theseupper motor neurons are going for the control of the hand,many more so than are going for the control of the feet. and she has particulardifficulty using her finger

flexors with her right arm. and he also goes on to testher mobility and her ability to resist movement andas well as her strength. so let's watch this examination. >> piece of paper put it in. good, again. that's pretty hard for thatlittle piece of paper isn't it? okay. >> here's our young lady again,

and she demonstrates atypical hemiparetic gait, and it affects only theright side of her body. typical of this gaitwith her weakness is that her arm is flexed, as isher hand as you saw before, and also her leg does not trackas well and it has to be brought out around and that iscalled circumduction. so she comes toward youher right leg has to veer out laterally so that itdoesn't scrape the floor because her foot is alittle bit more extended.

so extension of thelower limb and flexion of the upper limb iswhat you typically see with corticospinal tract damage. this gentleman has a hemipareticgait, just like the young lady. it affects his right side. her right side was affected too. her right side problemwas in her cortex. so that means herleft brain or pathway. this gentleman has a cervicalmyelopathy, so it's in the cord.

so that means it would bethe cord is being impinged on the same side producing thisweakness, his hand is flexed. he doesn't have theassociated movement of his arm comparedwith his left arm. recall corticospinal tractdamage is more to the extensor of the lower leg and theflexors of the upper extremity. to reinforce what you've justseen, this is an extreme example of a relatively recentstroke or infarct. on the right side of thescreen you can see damage

to the area of the motor cortex. and this would be a totalhemiparesis or paralysis, including all of theinternal capsule fibers that are descending tothe corticospinal tract. so this person would have hada contralateral hemiparesis or hemiparalysis in this case. this is a stained-myelincross section of the medulla. and the pale area onthe left, at the bottom, represents the area ofthe pyramid or pathway

some other structuresare also involved. this patient would have had asevere hemiparesis or paralysis on the opposite side, becausethe tract has not yet crossed. this is often called amedial medullary syndrome. before we leave thecorticospinal tract, i don't want you toforget that there are signs of lower motor neuron diseasethat we have not shown you, because they are moredifficult to show. atrophy is very obvious whenyou lose the lower motor neuron,

the spinal cord motor neurons, or even the cranialnerve motor neurons. and this is an example ofboth atrophy in the hand and in the muscles of the foot. this goes along witha loss of muscle tone, a flaccid paralysis, andloss of reflexes, areflexia. and sometimes in early stagesyou can see a quivering of the denervated musclecalled fasciculations. now it's time to moveon to the cerebellum.

so the cerebellum, togetherwith the basal ganglia, are merely consultants,so to speak, to the corticospinal tract orthe pyramidal system, all right. so your willed voluntarymovements before they occur, as they're goingon all the time, are consulting the basalganglia and the cerebellum. so let's focus rightnow on the cerebellum. an important thingis that disease of the cerebellum is manifest,shows up, on the same side

of the body as thepart of the hemisphere or midline that is damaged. so cerebellar lesions expressthemselves on the same side. that's just the oppositeof the corticospinal tract, which was on the oppositeside above the spinal cord. so that means that thecerebellar hemisphere has to work with the motorcortex of the opposite side. but we're going to focusjust on cerebellar disease. and we can dividethat into two regions.

the hemispheres that we saw and the anterior lobeand midline vermis. the anterior lobe andmidline vermis work more with the spinal cord. remember the spinal cordis constantly sending proprioceptive informationfrom muscle spindles, joints, tendons to the cerebellum. and the cerebellum iscomparing the state of the body, so to speak, with thedesire of the mind

to execute particularly fast,skilled, rapid movements. particularly things thatyou've learned to do with great precision,whether it's tennis or being a concert pianist. whereas the cerebellum anteriorlobe has more, much more to do with posture and gait andjust getting you balanced and carrying on withyour daily routine life. and so our damage isclustered as either problems with the hemisphere orproblems with the anterior lobe.

and so let's start withlooking at some examples of damage to the hemispheres. ataxia, or this incoordinationof the upper limb and or the lower limb, is atypical sign cerebellar disease of the hemisphere. this gentleman has difficultydoing what you call the finger-to-nose test. he has difficulty judgingthe distance, dysmetria, and he also has difficultydoing it in a rapid fashion.

he's doing it as fast as he can. and the examiner is moving thefinger a bit to make him stretch out and go to a differenttarget. you'll notice that superimposedon that movement is a tremor. so another typical sign of cerebellar disease is whatwe call intention tremor. it's only there when hetries to do something. it's not there at rest. let's look at another example.

this young woman has a problemof ataxia of her upper limb, but she has more of a dysmetriatrying to reach the target without past pointingas she is doing here. and she doesn't havethe big oscillations or intention tremor. but you do notice that she hasmore difficulty the closer she reaches the targetthat she is aiming for. so this is an exampleof lower limb ataxia. and it is also a sign ofhemisphere difficulty.

and this is calledthe heel-to-shin test. >> can you do thatone more time? high up right on the kneecap. and run it down the shinbone. okay, and i wantyou to use your heel like that and run it back up. let's go down for me. and back up on the shinbone. okay, good.

>> the physician here isasking the young lady to, as quickly as possible, flipher hands back and forth. and you'll noticethat she's clumsy. you can always compareit with yourself and how fast you can do it. and she has difficultyon both sides. and this inability to performrapid alternating movements is called dysdiadochokinesia. that's a real mouthful.

dysdiadochokinesia. and also the patient canbe asked to do rapid finger to thumb as fast as you can, and also that can beeither diminished or slowed. again, a problem withfast rapid movements. the last thing i wantto discuss with you about hemisphere diseaseis change in muscle tone. recall that with corticospinaltract we had spasticity, an increase in muscle tone.

and in cerebellar diseasesometimes, but not always, do you see a hypotoniaor a decrease in tone. and normally when you do areflex your opposing muscles, the antagonist muscles, tendto stop or check the movement. but in this case the legcontinues to wobble back and forth, and thisswinging is not checked and it is calledpendular reflexes. so pendular reflexesand hypotonia go along with cerebellar disease.

this woman has a hereditarycerebellar degeneration, which also affects theproprioceptive input to the anterior andvermian lobes and regions of the cerebellum. so as she walks she hasa classic ataxic gait and has to have assistance. this is a very severe example. and next i will showyou an example from a lesser-affectedindividual.

this woman also haspancerebellar degeneration. her gait is wide-based andshe requires assistance to keep her steady. but her disease is not asexaggerated at this point as the previous example. this patient has atumor in his cerebellum. it's only on one side. see if you can distinguishwhich is the affected side. remember, the disease, ifit's a cerebellar disease,

it's going to be in the sameside of the body as the tumor. and i think you can see thathe doesn't swing his right arm as much as his normal left arm,and that he has a broad gait to keep his balance, andthat he is an example of cerebellar ataxia, buta much more mild example. this gentleman has very severecerebellar degeneration. so much so that he wasunable to stand without help, and so he was placedon the bed here where we could recordhis postural tremors.

and this is called titubation,this oscillation of the trunk, axial titubation,or truncal ataxia. and it's so severe that it eveninvolves or invokes the movement of his legs and his head. again, an exampleof midline disease. one of the sequelaeof alcoholism over a long period time iscerebellar degeneration. we're looking now at a midsagittal sectionof the cerebellum.

and the left side, youcan see the shriveled or atrophied anterior lobe,and also it involves the vermis which is the cut surfacethat we're looking at here. so anterior lobe and vermiandegeneration are an effect of alcohol, among othercerebral problems. now why it affectsjust the anterior lobe and vermis, we don't know. but i'm going to nowshow you examples of when alcoholism issevere what are some

of the clinical signsthat you will see. this gentleman isgoing to be asked to perform the heel-to-shinmaneuver, which i just showedyou is an example of hemisphere involvement. but also the vermis and anteriorlobe represent more the lower limbs than the upper limbs. and so he has difficultyrunning his heel up and down over his shin andshows some deficit then

in his heel-to-shinmaneuver, on both sides. so this disease isof course bilateral. this same individual hasmuch less difficulty doing finger-to-nose thenheel-to-shin. and that is because alcoholism for some reason spares thehemispheres of the cerebellum, and they're more involved with the upper appendicularmusculature. so finger-to-nose is not acommon finding in alcoholism,

whereas the damageto the lower limb and its coordinationis more severe. when we were lookingat the diagram and list of cerebellar signsand symptoms, nystagmus was one of them. it can be cerebellar,it can be vestibular, or it can be brain stem. this young man shows aleft beating nystagmus. if you notice, hiseyes drift to the right

and flick back to the left. there are many formsof nystagmus. right, left, up,down and round about. but when you've seennystagmus, cerebellum or some of the connections to the cerebellum shouldbe in your diagnosis. we'll look at anotherexample now too. this gentleman also suffers fromspinocerebellar degeneration. and you're going to seeprominent nystagmus when he gets

to either the right side or theleft side when he's looking back and forth horizontally. his eyes do not move evenly. he doesn't have good pursuit. they're a little bitjerky if you compare them with your own eye movementsin the mirror or have, look at someone else's. so now we're ready to talkabout the other consultant to the motor cortex,the basal ganglia.

again, they do not have a directoutput to the spinal cord. they have to workthrough the motor cortex. they get there throughthe thalamus, just like the cerebellum does, and influence thecorticospinal tract. now, an important pointto remember here is that basal ganglia signsand symptoms that you see in the patient representdisease of the basal ganglia on the contralateral oropposite side of the body,

because the basal gangliawork with the cortex, because the cortex crossesin the corticospinal tract. the signs and symptoms ofbasal ganglia disease will be contralateral, just likethe signs and symptoms of cortical motor disease. now, because we havetwo pathways, a direct and indirect pathway in ananatomical sense, we had, we have two different typesof disease categories. we have diseases withtoo much movement,

which we call hyperkinesias,and we have diseases with too little movement,which we call hypokinesias. and we have some thatare a mixture of both. so first we're goingto look at diseases of the indirect pathway, which, because it normallyinhibited movement, now when it's diseasedwe get too much movement. and basal gangliadisease is categorized as a movement disorderand movement disorder

of involuntary movements. that is movements thatyou cannot suppress, that you cannot, concentratingas hard as you want, you might be able to diminishthem, you can't get rid of them. also an interplay betweenagonist and antagonist. and so we're goingto look at a variety of these movement disorders. too much, too little,or a mixture. and now we're going to lookat an example of athetosis

and a classic disease in the toomuch movement is huntington's disease, which has bothathetosis and chorea. unfortunately i do not havean example of hemiballismus, which involves disease ofthe subthalamic nucleus. and i do have examplesof iatrogenic or a medication induceddyskinesias, abnormal movements. let's look at some ofthese patients now. this is an example ofathetosis of the fingers. this gentleman is being askedto keep his hands still,

but his fingers still move. sometimes it looks likethey're trying to play a piano. and he's holding ontohis other hand trying to keep it under control. the sinusoidal movements arealways more distal than proximal and can be seen togetherwith chorea. this 51-year-old manhas huntington's disease and shows a good exampleof a choreiform gait. notice that it's intrudedupon by movements of his hands

and his shoulders,his hip, his knee, that are unintentionaland unwanted. unfortunately, this autosomaldominant disease manifests itself later in lifeafter child rearing years and childbearing yearshave come to pass. this unfortunate woman alsohas huntington's disease. and she's just asked to prettymuch sit still and stand still. but you can see the intrusionof all of these movements, and it makes it difficult forher to speak and is exhausting.

unfortunately this diseasealso carries with it dementia. it's called a subcorticaldementia because it's not necessarilyonly in the cortex; it involves these basalganglia structures, which are involved in cognition. so this is an exampleof a severe stage of huntington's disease. what we're going to look at noware iatrogenic, or drug induced in this case, dyskinesias,

sometimes they're calledtardive dyskinesias. they come on after long termparticularly antipsychotic medications and arecalled orobuccal and sometimes lingualorobuccal lingual dyskinesias from long-term drug effects,and they are often irreversible. so this is somethingyou want to keep in mind when using certain medications. tardive dyskinesias. now let's listen to him.

dyskinesias can also come from long term parkinson'sdisease medication, as you're going tosee in this woman. she has movements, but they'renot of the orobuccal type. they are other partsof her body. it is quite disconcerting, and you can see she iscontinuously agitated. >> well, i take it twice, 5:30,and about 6:30 to about 8:00 or 9:00 is my mostproductive time.

>> finally we're readyto discuss the last part of our involuntarymovement disorders, those that causetoo little movement. diseases of the direct pathway. and these are calledhypokinesias. let's look at some of them. patients with parkinson'sdisease have a change in their muscle tone. it's not spasticityit's rigidity.

it's stiff in alldirections of movement. and sometimes this is referredto as leadpipe rigidity. let's watch this examination. >> i'm going to check to seehow stiff your muscles are. i want you to relax. yes, wet as a noodle. just relax. >> he's having adifficult time moving it, no matter what directionor at what speed.

and if you watch thewrist there's a little bit of a catch in it. and sometimes that iscalled cogwheel rigidity. cogwheel rigidity,as if they were going through little notchesin a gear. >> have this hand. >> notice that thehand doesn't flop. it's stiff. this gentleman isgoing to demonstrate

for you the very typicalparkinsonian gait, which is a shuffle with smallsteps, difficulty initiating it, called bradykinesia, anddifficulty turning with lots of small steps, sometimesreferred to when severe as in en bloc turning. notice that he doesn't movehis arms very much as he walks. notice his stooped posture. and if you could see his face, his face is practicallyexpressionless

with very little blinking. now let's watch his examination. >> walk back. make a quick turn for me. walk. come back. >> this 74-year-old gentlemanalso has parkinson's disease. and you're going to see that hisone arm has greater difficulty in movements, both of thearm, the hand and the fingers. this asymmetry is oftentypical in the presentation

and eventual evolutionof parkinson's disease. and we're going to watch him. and you'll notice thathe also has a tremor. this differs fromcerebellar tremor. this is called resting tremor. so the tremor is there whenhe is not doing something, but the minute commanded todo it, it either disappears or decreases significantly. let's watch him.

>> i'd like for you to putyour hands out in front of you, and spread your fingers apart. good. and take that indexfinger and touch your nose. >> you see, when he's toldto do something it stops, but then when he hashis arms extended at rest it begins again. now he's going to do thefinger-to-nose maneuver. and you see the tremor decreases when he's doing somethingintentionally.

so this is a restingtremor that he has. if this were cerebellardisease he would have dysmetria and intention tremor. his hand up there at restwhile he's doing something else with the other arm. and you can see thatthe tremor returns. he also has sometremor in the leg. we're going to look at whatis called retropulsion. because the patient hasdifficulty initiating movements,

his response time to a gentlepush forward or backward or to the right orleft is delayed so that they often tend to fall. so this retropulsion is anexample of that bradykinesia and stiffness of his movements. >> i'm going to giveyou a little push. i'm going to push youforwards, sideways or backwards. and i'll be here to hold you;i won't let you fall, okay. okay, and you try tohold your position there.

>> it's the backwardsthat's harder. >> one more time. >> see, it's worsegoing backwards. a very easy test. >> doing great. >> so this concludesour discussion and comparison ofthe motor systems. remembering that thecorticospinal tract trumps everything.

if it's not working, then youwill not see the subtle basal ganglia and cerebellar signsbecause of the hemiparesis, paralysis and lackof motor control. however, if the corticospinaltract is working and you see diseasethat is motor, think, is it an involuntary movement that the patienthas no control over? and if so, is it too muchmovement or abnormal movements? think basal ganglia,particularly

if there is a resting tremor. on the other hand,if the problem comes with doing motor acts and it'suncoordinated, think ataxia. and if there is a tremorduring the movement or action that is ataxic, you wantto think cerebellum. so maybe these motor circuitswill be a little easier for you to remember now that you've seensome of these clinical examples.