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Related readings Blumenfeld pgs 5960 76 472473 529 558 567572 673674 2008 Week 6 Molar Systems 5 39 Eye movements S Perlmutter O bj ectives to describe the location and action of the extraocular muscles to describe the location of extraocular motoneurons and the course of their axons to understand the cause of internuclear ophthalmoplegia to understand the function and neural pathways of the vestibuloocular re ex to de ne nystagmus to understand the effect of vestibular lesions on eye movements to understand the function and neural pathways of the optokinetic re ex to describe the 3 types of voluntary eye movements to describe the neural pathways for saccades to understand the function of the superior colliculus for saccades to describe the neural pathways for smoothpursuit eye movements to understand how vergence eye movements differ from other types of eye move ments and how they are associated with accommodation Weeks 11 Figure 1 Su n rmd S m Extraocutarmusctesarespectattzedsketetat P 5 Fem 5 mth es e g t ttoertypes ottterent than ttmo musctes a as et more energy eman tt tg Superinr Superior oblique oblique a Media Linus on the posttton of the the body even stmpte eye movements for can rectutt39e the ooorotnateo oontraotton of utttpte extraocutar m sotes tt t aott hsofth extr t Laterat tus m t h ey 2 eotat rectth muscte adducts the eye 3 Supertor rectth muscte pnmanty etevates the e e 39 4 thfertorrectus muscte pnmanty depresses the e e 5 Su ertot39obttquemuscte producestntorston and depresston of the e e 6 thfet39tot39obttctue muscte produces extorstot39t and etevatton orthe e e The e e ts a much stmpter meohantoat system than the sketetoh evtraooutar musctes do not need to tan posture or staotttze totnts ttke other sketetat musctes 39 V mans Supertur vtew su vts on Figure 2 dirsat d t Motoneurons for extraocutar musc es h ettm e ta e are tooateo tn 3 huctet on each stoe of the ven ta pSt m a rec bratnstem medtat oontrataterat supertor rectth 1 The ocutomotot39 t tucteus tteS hearthe mtdttt te tn the mtdbt att t tt h854 Subdtvtstot t t ocutomotor hucteus the bratnstem just medtat to the cerebrat trochtear hucteus u o 1 z 3 g 3 5 3 o 0a Q m 2 3 o 2 o o o tttro nerve protects ocutomotor Just postenor to the ooutomotornuoteus nerve Ht t5 r ht rhu te s Whtch m ates the oontrataterat Supertor obttque vta the quotMeta tvt ramat nerv Axe n neNeW I a t tucteus ah eXtt e orsat S bratt tstem behtt td he tt tfertot cotttcutus abducet ts hucteus 3 The abducet ta hucteuS ttes atthetuhcttoh po 5 and medutat medtat and a btt rostrat to the yeattbutat huctet tt whenates the atet at rectLtS muse v a the Vtth crantat Postertor VIEW nerve Nona run yehtt at and taterat to extt the ventrat Surface ofthe bratt tstem abducehs nerve Vt NOTE AKth otsupenorreotus and supertor obttque motoheurohs cross the mtottne Antermr mew Week6 12 ur Locati n of ocmomotor trooh ea and abducens nude m crossrsectwons ofthe bramstem Caudal pons or COWCMUS Trochlear Oerebra nucleus 3 new 5 VTrochIear 1 V nerveV Caudal V midbrain J DecLssann ofsupe r oerebeHar pedunc e Eupenov cdhcu us Rostral midbrain Oculomotor nervelll Week6 13 Figure 4 The tunotton otthe abducens nudeth and the rneotat rectth suoowtston tthe ooutornotor nudeth are coordtnated roup of neurons m the abducens rn n hortzontaHymtan ern The axons projectmg from the abducens g o z a o o g a 1 i 3 E Q o o a be travet m the rneotat tongttuotnat tasotoutus mm a targe bertrack travehng nearthe rntohne for hearty the enttre tength of the bratnstem tnternuotear noers are omy a smaH component otthe MLF r trauma that Sever the MLF o 0 E0 0 3 0 two e oenot e tntemudear oothatrnootegta an eye cannot rotate nasaHy mat the oentrat pomuon Figure 5 Damage to the nerves mnervatmg the vergence movements Week6 14 A A Alma 7 reclu5 Omhmmtur nucleu M dial Miamiquot Inngilmhmt k culne ppm ATTENPTINE YD LDEIK T THE RIGHT Len lnlzrnucle r ophthalmnmegia Vergence O K Laft culnmnlnr Nerve Pnlgu Vergence impaired Right Ah ucens Nerve Palsy Figure 6 ates vtsuat acuttvts not good tommages that faH outstde the fovea and when tmages move across the rettna Two compensatom tmprove vtston ov keeptng tmages staote on the rettna 2020 Visual netds cl ten eye Figure 1 Acttvatton of vesttoutar oanat or otohth e eptors produ s the vestibuloocular head velocny tqu W Hutsm KCuHen Inn 50 ms 25 Hz too degs movements m wmc eves move m the same dtrectton are caHed con39ugate mmmguts head vam39y aavamy thmtvoa C 201 00 0200 2 1 2mm visuat tietds ot tight eye LtstvEEYK Pavstku 1586 eye Velocity head Velocity 30 degs 100 ms Fukusmma 1557 Week6 15 Figure 8 thh targe head rotattons such as 3607 degree body turn th OR e ttwar beaung nys tagmuae stow phasesto the Hgm tast phases to the tett Figure 9 Thevesttbutoocutat re ex ts produced when vest butarreceptots acuvate neurons inthe t39 uc eus a o39e 39 tater t t ctus sde and nt mudear neu onsprotec t eMLFt tattectus to em mt ett to tornudeus mo n contracttngthetettrnedtat rectus Equwatent pathways ongtnatt n the nght honz n at are tnh btt ng t o t serntchcutar canats whtch ed b dc an ereb vest bu oocu ar re exes Week6 16 gt Recordmg etectmdes T 9 gt 39 gt D A 4 quot quot 143 Fastuhases D A C I 1 Honzonla eye pnsihon Slow phases VESllhlllnl39 nuclei vestibular and M Vllllh nerve R yIJ hnriznnl l semicircular agents 7 HEAD TURNING I LEFr lwn Darts 01 nh ucens nucleus L nculnmnlnr nervewn nerveull L Figure 10 Because vestroutararterehts ththe vestoutar at a steady background rate W the oh ohe st e t5 t5 turbed The background dtscharge W the tow the arhaged st e a tftheh ad t5 atmgt stde r eth e shoe thrs mappropnate d ve t5 COHUHUOUS e U at hta u vestrutar nystagmus ensues dhtrt the Draw adapts hours or days 11 he seeohd oeutar re ex drtves the eyes h ve h a targe vrsuat hmtt h the o r e eyes esetthh td OUOH ht oooste dtrectton produ r optoktneltcnystagmu Th oot ktnettcre ex het s the Stabmze vtston duh hg ea vements tn the hght The optoktnehc re ex produces Conjugate eye movements The pathwaymedtattng the optokmehc re ex oegrhs thh strrhutattoh of Wtder etd rethat g s hprotectto se te oohtrhe retreutartorrhatroh ahd thevest outar regtons otthe cerebeHum a VESTIBULAR NERVE LESIHH NYSTAGMUS vestibular part of Vlllth nerve eye nast an NVSTAEHLIS Igt gt alnw phuae tothanght lt 1 time Simwan to the ten rust nhase J oflhe optic tract Oculomolor lrochlear abducens nuclei Week6 17 Figure 12 There are 3 types of voluntary eye movements saccades smooth pursuit and vergence Saccades are rapid conjugate eye movements used to direct gaze from one target of interest to another Saccades are ballistic and completely preprogrammed once they start they progess to their end without modification Saccades are very brief 15 ms for small saccade 60 ms for large ones and very fast They have a latency typical for voluntary movements 150200 ms Humans make 10s or 100s of thousands of saccades each day In the figure the eye position trace is offset downward a small amount for clarity the eyes actually look directly at the target Figure 13 Voluntary eye movements are initiated by several regions of the cerebral cortex The frontal eye fields and supplemental eye 39 are located rostral to the primary o 1 D 3 3 c 3 8 o 3 m 2 D lt D 3 o lt D 3 D 3 m analogous to those of primary motor cortex and supplementary motor area for limb movements These areas contain motor maps for contralateral saccades The maps represent movements in visual space rather than movements of body parts Electrical stimulation at a given site produces a saccade that points the eyes to a location in the contralateral visual field The parietal eye fields are involved in the selection of visual targets direction of attention and the determination of the position of targets in bodycentered space ie independent of where the eyes are pointing The three cortical eye fields are reciprocally connected Week6 18 Right Supplemental precentra sulcus central sulcus Parietal eye field Visual Frontal association eye field cortex gr colliculus IS another A Superior Collicuclus Motor Map dorsal View important structure for the control of saccades The superior colliculus is center of Len usual Righl a layered structure in the midbrain 9323 I superficial layers have visual sensory properties and deeper layers have motor vertical properties The deep layers contain meridian another motor map of contralateral visual space Electrical stimulation at specific sites A produces saccades to specific locations in space B as shown in the 720 figure Neurons at these sites burst hOIIZOIIIaI prior to voluntary saccades to the same mendlan locations B Eye Movements Elicited by Stimulating the SC Left Right vertical meridian 20 Wl39iite circles are Visual Up 6 receptive elds l i 0 center ofgaze arrows are eye DOWI l movements Figure 15 evoked b The superior colliculus and the cortical eye 720 SIImLJIatIngII ie SC fields project to regions in the brainstem at corresponding that activate extraocular motoneurons for numbered sites above saccades There are separate regions I I I I for horizontal and vertical saccades The 30 20 09 720 730 horizontal gaze center is located in the paramedian pontine reticular formation PPRF near the abducens nucleus The vertical gaze center is located in the interstitial nuclei near the oculomotor abducens nucleus midbrain 9139 mediate Week 6 19 6 Saccades dwfferent target ocahons are t ropnate durabon a tempora representatbn m specmc motoneurons to move the eyes to the target e neural pathway that executes nuc eus are 5 50 nvo ved we ab cens mtemuc earmtemeur n5 Vemca saccades are controHed by snnnarcncuus nvo vmg the rmdbram gaze center Week 6 20 eJerw llolherlghl HHHHHHHHIIHIIHH H H g 9 rate deterrmnes burst of nnng durmg new steadyt Josmon of eye by saccade rapwd comracts rate ho ds m a pamcu ar mew rectus durauon of new nonzon mem rermlt mmr e bum de ermmm nnwmr Supp ememz Eye He d Par etz anlal Eye He d Eye F El Cembia Co ex Supenuv Colhcmus Cerebenum removcdl Figure 13 Smooth ursuit eye movements are slovy E S e lt o o 3 z to 3 o o 3 o a z o 1 8 l5 able to generate mostly a Series of small saccades Figure 19 The neural pathway for smooth pursuit u nucleus affects each ofthese eye movement Smooth pursuit example r39 20o eye rotation 1 second quotME 100 msec E 5 deg eye position B target Frontal eye field Visual cortex Lateral geniculatei nucleus Oculomotor trochlear abducens nuclei l MLF gt0ntine iuclei lt Cerebellum W Vestibular nucleus Week 6 21 Review Blumenfeld ch 181 pp 780787 KCC 1921910 pp 82947 This article originally appeared in Introduction to Basic Neurology by HD Patton JW Sundsten WE Grill and PD Swanson pp 33242 1974 WB Saunders Company and is used here at the request of the author 2008 Week7 Higher cognitive function Clinical perspectives P Swanson Objectives 0 to understand where language and memory localize to name some disconnection syndromes 0 to name the features for several types of aphasia SPEECH AND SPATIAL PERCEPTION It is well known that the majority of people are more dexterous with one hand usually the right than with the other A person with an infarction or other lesion in the brain is much more likely to have a disorder of language aphasia when the lesion is located in the left cerebral hemisphere than in the right These two facts have given rise to the concept of the dominance of the left cerebral hemisphere over the other There have also been observations that suggest that lesions in certain parts of the dominant hemisphere are more likely to cause aphasia than lesions in other parts are More over the type of speech disorder may differ according to where the lesion lies Some patients who have lesions in a cerebral hemisphere may have problems of perception rather than or in addition to speech disorders such as inattention to stimuli on the side opposite the involved hemisphere spatial disorientation or failure to recognize common objects in the environment agnosia Although some of the latter functions can be investigated in animals it is obvious that study of speech mechanisms must depend upon observation of humans It is important to remember that as is also true of other symptoms or signs due to damage to the central nervous system aphasias can be mild or severe depending on the location of the pathologic lesion on the acuteness of the damage and often on the length of time that has passed since the damage occurred Thus infarction of a part of the left cerebral hemisphere may initially cause profound dif culty with use or understanding of words After days or weeks improvement may be striking so that the patient has very little de cit It may be dif cult to predict ace curately the ultimate extent of recovery since some unfortunate persons may improve very little Probably it is correct to state that the earlier the onset of improvement the better the ultimate prognosis Anatomicaleclinical correlations are obviously not always very precise since the same lesion may be associated with aphasia of severe or mild degree depending on the time of observation Improvement in speech may also be attributed erroneously to whatever therapeutic measures are being employed Speech disorders have been examined in most detail in patients with brain damage due either to infarction or to trauma Even in leftehanded individuals the left hemisphere is usually the more important hemisphere for speech Anatomically in 65 per cent of brains a portion of the superior surface of the temporal lobe appears to be larger in the left hemisphere than in the right hemisphere Fig 251 and this area may be one of those that have particular importance for speech This anatomical area is located behind the transverse gyrus Heschl 39s gyrus which receives auditory information from both ears Asymmetry of size of these cortical regions is evident even in newborn infants suggesting that anatomical specialization is a builtein feature of the cerebral hemispheres Another important anatomical area for speech is located in the region of the operculum of the frontal lobe Broca 39s area Other parts of the left cerebral cortex in the temporal and parietal lobes are also considered important for speech Fig 2572 Week 7 35 Week 7 38 Clinical Cases able to write his own name and address but could not write that of his mother He could not count but could write numbers to 21 When asked to write a simple phrase to dicta tion he frequently failed to nish the sentence Seven months after the injury he still had great dif culty with verbalization He was able to name objects well but in spontaneous speech he had great dif culty in evoking words Pronunciation was poor Writing was done with dif culty with defective word formation Seven years later he still hesitated in nding words and showed defective enunciation and uency in writing Though there was no pathologic con rmation of the site of damage this patient39s aphai sia would be termed a non uent expressive or Broca39s aphasia Care N0 2 A 557yeariold woman developed dif culties with speech over a period of several weeks Her complaint was I didn39t have any memory in my arms or even to talk I39d lost the ability to talk I have lost all the use of the people I knew except my own family and people I know real well that39s ne I know them but many many people I used to know I don 39t have their names There is a little bit of the regular things that l have lost the use of some articles that I can 39t think of the name ofquot On examination she was able to talk rapidly with long sentences Most words were pronounced well though she would occasionally substitute a word or a phrase that was 5 without spelling errors and she could calculate with little dif culty Her most profound 39 culty was an almost complete inability to name simple objects such as a piece of chalk a key a pencil She would say Oh I should know now what39s the matter I thought I knewquot At times she would use an incorrect adjective She was better able to nd the correct name for a coin but even here she sometimes was uncertain that the word she chose was correct Shown a pair of glasses she said It39s what you look out of I know what it 39s used for and everything but I cannot remember that name It 39s used to see throughquot This patient was found to have a gliomatous tumor in the left temporal lobe Her aphasia was uent or receptive and to a large degree could be characterized as a nominal o anomic aphasia speech and inability to name objects are found when stimulation is in the region of the nuclei of the left thalamus DISCONNECTION SYNDROMES Some important studies were canied out on patients who had undergone section of the corpus callosum as a treatment for epilepsy This procedure is very rarely performed even by neurosurgeons with special interests in the sur 39cal treatment of epile sy the patients appeared quite normal being able to swim catch objects with both han Figure 253 Diagram of visualtactile association test in splitbrain subject The subject focuses on the center of the screen A picture of a spoon is flashed on the left side ofthe screen activating the right visual cortex with the left hand the subject palpates objects below the table top and retrieves the spoon Tactile information from the left hand projects mainly to the right hemisphere the weak ipsilateral projection dotted line being inadequate for the subject to name the object selected using only the left hemisphere From The Split Brain in Man by Michael S Gazzaniga Copyright c 1967 by Scientific American Inc All rights reserved Un A or light a cigarette In special test situations however it could be demonstrated that the two hemispheres were functioning quite independently Fig 25 3 It was found that if a patient had something placed in the right hand or if an image was projected only into the right visual eld therefore going via the left half of the retina into the left cerebral hemisphere he was able to verbalize the name of the object he had felt in his hand or seen in his right visual eld In contrast if an image was ashed in the left half of the visual eld information ultimately reaching the right hemisphere the patient denied seeing the image However when the patient was directed to nd with his left hand the object that he had seen he was able to do this His inability to report verbally about the visual input to the right hemisphere was due to the fact that he was unable to transfer the information in his right hemisphere over to the speech centers located in the left hemi sphere Similar ndings occur when such a patient attempts to identify objects placed in the hand If something is put into the left hand he can match it on a nonverbal test but is unable to verbalize what he has felt This indicates that the left hemisphere is indeed dominant for speech Certain clinical syndromes are sometimes encountered in which the symptoms are due in part to disconnection of one area of the brain from another One such syndrome is characterized by alexia word blindness without agraphia in which the patient has the ability to write but is unable to read The patient also usually has a right homonymous hemianopsia but is able to name and recognize objects This syndrome can occur with combined infarctions of the left primary visual cortex and the splenium of the corpus callosum sometimes as a consequence of occlusion of the left posterior cerebral artery Visual information comes to the right cerebral hemisphere but cannot be transferred to the left hemisphere and gain access to those parieto occipital areas necessary for recognition of words How can such an individual visually recognize objects other than words The reason for this discrepancy is not certain but is suggested to be due to the nonverbal associations evoked by visual objects touch taste smell allowing transfer of information across callosal bers located more anteriorly Another rare but instructive disconnection syndrome has been described in patients with destruction of the anterior four fths of the corpus callosum due to ischemia in territo ries of branches of the anterior cerebral arteries Visual information can pass between the two occipital lobes so the patient can read in either visual eld An object held in the left hand cannot be named however since the somesthetic information from the right hemisphere cannot reach the left hemisphere speech centers The patient cannot A rite correctly with the left hand or carry out commands with the left hand because of inac cessibility of verbal information to the right hemisphere Week 7 39 TABLE 252 Classi cation of Memory duration of recall how tested immediate recall seconds repeat numbers recall names of objects shortiterm memory minutes to hours recall names of objects or events of the recent past even after a distraction longiterm memory months to years recall events remote in time in performing well He denied being ill and said he was in the hospital because his wife thought he had had a stroke The only motor abnormalities were a mild weakness of the left face and some loss of precision on doing ne movements with the left hand He performed accurately on testing of pinprick light touch position and vibration sense He could identify objects placed in his hands He had similar dif culty on both sides with gureiwriting on the skin However when touched on both sides simultaneously he always denied feeling the stimulus on the left side even when the stimulus occurred in the left eld of vision He was able to read and write and his speech was normal He could not draw the simplest object accurately failed to close a square and put the numbers of a clock face outside the boundaries of the face The inaccuracy was more pronounced on the left side of the drawn object He drew a very inaccurate map of the state of Washington andpaid little attention to boundaries that he drew Asked to ll in gaps in a simple incomplete drawing of a face he ignored the absence of the right eye to the patient 39s left When inaccuracies were pointed out to him he became somewhat hostile and asked the exam iner to try to do better if he thought he could THE NEUROLOGICAL BASIS OF MEMORY The ability to remember information that has been learned or experienced minutes days or years before is perhaps the most important function of the brain We remain at a very primitive level of quot both the 39 39 and 39 bases of memory though there are indications that certain anatomical regions are important for memory consolidation and recall One problem that faces the student of learning and memory is the dif culty in reconciling information obtained from animal studies with that obtained from examination of humans For example in humans damage to the medial portions of the temporal lobes including the hippocampal regions can be associ7 ated with profound memory de cits whereas ablation of such regions in experimental animals may not alter performance on learning tests Part of the problem may be due to dif culties in precisely subclassifying the varying types of memory One classi cation differentiates memory into groups depending upon the interval between learning the information and recalling it as in Table 2572 Clearly there are very broad time zones involved and deciding at what point shortiterrn memory blends into longiterm memory is impossible Even such a broad distinction is useful however since in certain situations one type of memory may be disturbed without effects on another Certain clinical conditions encountered in man can be associ7 ated with rather striking de cits in the ability to learn and to recall recent events This is called the amnestic or amnesic syndrome or Korsakoff 39s psychosis and is encoun7 tered in patients who have had bilateral damage to particular areas of the cerebral hemispheres In humans the medial portions of the temporal lobes including the hippocampal com plexes are generally accepted as being critical for memory formation Agreement is less about the importance of connected areas such as the fomix and mammillary bodies though the brain of a patient with an arnnestic syndrome due to thiamine de ciency will usually be found to have damage to the mammillary bodies These areas appear to be of importance for the formation of a lasting record of events in other parts of the brain and for retrieval of memories from storage There have been several reports of marked de cits of memory in patients who have had surgical removal of both temporal lobes as a treatment for epilepsy and in patients with Week 7 41 Figure 255 Bilateral infarction of the hippocampus in a patient with severe memor loss A Transverse section of the brain at the level of the lateral geniculate bodies Arrows point to necrotic hippocampus B Microscopic section showing chronic infarct of Ammon s horn CA and of parahippocampal and fusiform gyri F From DeJong et at Arch Neurol 1969 20 339348 Week 7 42 12 occlusions of both posterior cerebral arteries resulting in infarction of the medial pori tions of the temporal lobes including the hippocampus Fig 255 A 297yeariold patient of Scoville and Milner 1957 had been incapacitated by in tractable seizures since the age of 16 and was subjected to a neurosurgical procedure At operation the mesial surfaces of both temporal lobes were resected to about 8 cm posteriorly from the temporal tips After operation this young man could no longer recognize the hospital staff nor nd his way to the bathroom and he seemed to recall nothing of the dayrtoiday events of his hospital life There was also a partial retrograde amnesia inasmuch as he did not remember the death of a favorite uncle 3 years previously nor anything of the period in the hospital yet could recall some trivial events that had occurred just before his adrnisi sion to the hospital His early memories were apparently vivid and intact Even after 3 years this patient was unable either to learn a new address or to remember where objects in continued use were located His memory de cit was the more remark able since his intelligence quotient was 112 prior to operation it had been recorded as 104 He appeared to a casual observer as relatively normal since his understanding and reasoning were undiminished He could retain a threei gure number or a pair of unrelated words for several minutes if undistracted but if his attention was drawn to a new topic they were immediately forgotten Psychological testing failed to reveal any de cits in either perception abstract thinking motivation or personality Patients who have suchlesions have dif culty in the process of storing memories They can immediately remember a task immediate recall but are unable to consolidate it suf ciently to remember it a few minutes later These patients are virtually unable to establish lasting new memories although they can remember things that they have learned long before and may be able to remember small bits of information perfectly for seconds or a few minutes if undistracted This type of memory consolidation which requires the presence of the temporal lobes is termedrecent memory and is to be con trasted with longiterm memory which may not be dependent on the hippocampal areas In animals for example lesions of the hippocampus that have been made a few days after the learning of a maze cause severe impairment in performance Lesions made 6 or more days after learning produce no impairment in maze running thus it would appear that the memory tracequot has become independent of the hippocampus Implication of the hippocampal formation rather than either the parahippocampal cortex amygdaloid nucleus or uncus is strengthened by isolated cases of memory loss associ7 ated with discrete infarctions of both hippocampi with sparing of these other areas These regions lie in the supply tenitories of the posterior cerebral arteries and can be damaged with occlusion of these arteries by either thrombi or emboli When an amnesic syndrome occurs after a unilateral temporal lobectomy it is usually assumed that prior damage has been present in the other hippocampal region so that bilateral hippocampal dysfunction has resulted In fact the majority of patients with uni lateral temporal lobectomies do not develop severe memory loss Occasionally however a loss of recent memory occurs after unilateral temporal lobectomy One such patient became amnesic at age 46 after removal of the left hippocampus 5 years after removal of the anterior 4 cm of the same temporal lobe At autopsy the remaining right hippocami pus was shrunken pale and rm and there was severe loss of neurons in the pyramidal cell layer These de ciencies probably occur at the time of birth and are frequently found in the brains of patients who have psychomotor seizures Only rarely has a profound memory disturbance occurred after damage to one cerebral hemisphere with pathologically con rmed absence of damage to the other side One such patient had an extensive infarction in the territory of the left posterior cerebral are tery Caplan and Hedley7Whyte 1974 She could write but was unable to read alexia had dif culty with calculations and with visual object andpicture identi cation and showed a severe defect in recent memory function During the acute phase of her illness she could recall I or 2 facts in a 107part story after 3 min but almost nothing of the story after 10 min She could not recall being in a special room on 12 different occasions Her memory gradually improved so that after 7 months she could remember names and could report 7 of 10 facts of a story given 10 min before She never regained memory for the onset of her illness or for events during her rst hospital months The infarction included gray and white matter of the medial temporal lobe extending into the occipital lobe and including the splenium of the corpus callosurn the posterior hippocampus and geniculate bodies An infarct was also present in the posteroventral lateral nucleus of the left thalamus The left fomix and mammillary body were atrophic It is possible that memory disturbance is more likely to occur with a unilateral lesion if the thalamus is involved in addition to the dominant temporal lobe When one goes beyond these anatomical considerations discussions of memory mecha7 nisms become even more dif cult to relate to known physiological or biochemical phe nomena Memory consolidation may be impaired by electroshock However after deep coma brought about by overdoses of sedative drugs patients may remember events up to the time of drug ingestion Persistence of memories may be found even after almost complete cessation of the electrical activity of the brain This makes it unlikely that memory storage can be accounted for by reverberating electrical circuits The establish ment of memory traces must involve structural change that persists beyond the event that is remembered Evidence is accumulating that a certain amount of plasticity exists at the level of ne nerve terminals which can be demonstrated in electron rnicrographs to innervate areas that have been deprived of incoming connections Much of the biochemical work on memory has been dif th to reproduce and there are widely divergent ideas about the chemical changes that occur with the making of meme ory The most speculative workers envisage memory molecules that range from peptides to ribonucleic acid RNA and that code for speci c memories Claims of transfer of memories between animals and sometimes across species lines seem incredible Less imaginative but perhaps more likely to be correct are the suggestions that biochemical changes at the synaptic level might occur in association with establishment of new and more lasting connections among nerve circuits Week 7 43 Week 7 44
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