The occipital The occipital lobes Occipital lobe - Mahidol University

23/06/54NEUROPSYCHIATRY 17 NEUROPSYCHIATRY 183

23/06/54NEUROPSYCHIATRY 19NEUROPSYCHIATRY 22NEUROPSYCHIATRY 23Spatial encodingThe retina, unlike a camera, does not simply send a picture to the brain. Theretina spatially encodes (compresses) the image to fit the limited capacity of theoptic nerve. Compression is necessary because there are 100 times morePhotoreceptor cells than ganglion cells as mentioned above. The retina does soby "decorrelating" the incoming images in a manner to be described below.These operations are carried out by the center surround structures asimplemented by the bipolar and ganglion cells.There are two types of center surround structures in the retina—on‐centers andoff‐centers. On‐centers have a positively weighted center and a negativelyweighted surround. Off‐centers are just the opposite. Positive weighting is morecommonly known as excitatory and negative weighting is more commonly knownas inhibitory.These center surround structures are not physical in the sense that you cannotsee them by staining samples of tissue and examining the retina's anatomy. Thecenter surround structures are logical (i.e., mathematically abstract) in the sensethat they depend on the connection strengths between ganglion and bipolarcells. It is believed that the connection strengths between cells is caused by thenumber and types of ion channels embedded in the synapses between theganglion and bipolar cells. Stephen Kuffler in the 1950s was the first person tobegin to understand these center surround structures in the retina of cats.4

23/06/54The visual cortex of the brain is that part of thecerebral cortex responsible for processing visualinformation. It is located in the occipital lobe, in the backof the brain.The term visual cortex refers to the primary visual cortex(also known as striate cortex or V1) and extrastriate visualcortical areas such as V2, , V3, , V4, , and V5. The primaryvisual cortex is anatomically equivalent to Brodmann area17, or BA17. The extrastriate cortical areas consist ofBrodmann area 18 and Brodmann area 19.There is a visual cortex in each hemisphere of the brain.The left hemisphere visual cortex receives signals from theright visual field and the right visual cortex from the leftvisual field.Visual Cortical SimpleCell6

23/06/54Third visual complex, including area V3The term third visual complex refers to the region of cortex located immediately in front of V2, whichincludes the region named visual area V3 in humans. The "complex" nomenclature is justified by thefact that some controversy still exists regarding the exact extent of area V3, with some researchersproposing that the cortex located in front of V2 may include two or three functional subdivisions. Forexample, David Van Essen and others (1986) have proposed that the existence of a "dorsal V3" in theupper part of the cerebral hemisphere, which is distinct from the "ventral V3" (or ventral posteriorarea, VP) located in the lower part of the brain. Dorsal and ventral V3 have distinct connections withother parts of the brain, appear different in sections stained with a variety of methods, and containneurons that respond to different combinations of visual stimulus (for example, colour‐selectiveneurons are more common in the ventral V3). Additional subdivisions, including V3A and V3B havealso been reported in humans. These subdivisions are located near dorsal V3, but do not adjoin V2.Dorsal V3 is normally considered to be part of the dorsal stream, receiving inputs from V2 and fromthe primary visual area and projecting to the posterior parietal cortex. It may be anatomically locatedin Brodmann area 19. Recent work with fMRI has suggested that area V3/V3A may play a role in theprocessing of global motion Other studies prefer to consider dorsal V3 as part of a larger area, namedthe dorsomedial area (DM), which contains a representation of the entire visual field. Neurons in areaDM respond to coherent motion of large patterns covering extensive portions of the visual field (Luiand collaborators, 2006).Ventral V3 (VP), has much weaker connections from the primary visual area, and stronger connectionswith the inferior temporal cortex. While earlier studies proposed that VP only contained arepresentation of the upper part of the visual field (above the point of fixation), more recent workindicates that this area is more extensive than previously appreciated, and like other visual areas itmay contain a complete visual representation. The revised, more extensive VP is referred to as theventrolateral posterior area (VLP) by Rosa and Tweedale.Visual area V4 is one of the visual areas in the extrastriate visual cortex. It is located anterior toV2 and posterior to posterior inferotemporal area (PIT). It comprises at least four regions (left and rightV4d, left and right V4v), and some groups report that it contains rostral and caudal subdivisions as well.It is unknown what the human homologue of V4 is, and this issue is currently the subject of muchscrutiny.V4 is the third cortical area in the ventral stream, receiving strong feedforward input from V2 andsending strong connections to the PIT. It also receives direct inputs from V1, especially for centralspace. In addition, it has weaker connections to V5 and dorsal prelunate gyrus (DP).V4 is the first area in the ventral stream to show strong attentional modulation. Most studies indicatethat selective attention can change firing rates in V4 by about 20%. A seminal paper by Moran andDesimone characterizing these effects was the first paper to find attention effects anywhere in thevisual cortex.Like V1, V4 is tuned for orientation, spatial frequency, and color. Unlike V1, V4 is tuned for objectfeatures of intermediate complexity, like simple geometric shapes, although no one has developed afull parametric description of the tuning space for V4. Visual area V4 is not tuned for complex objectssuch as faces, as areas in the inferotemporal cortex are.The firing properties of V4 were first described by Semir Zeki in the late 1970s, who also named thearea. Before that, V4 was known by its anatomical description, the prelunate gyrus. Originally, Zekiargued that the purpose of V4 was to process color information. Work in the early 1980s provedthat V4 was as directly involved in form recognition as earlier cortical areas. This research supportedthe Two Streams hypothesis, first presented by Ungerleider and Mishkin in 1982.Recent work has shown that V4 exhibits long‐term plasticity, encodes stimulus salience, is gated bysignals coming from the frontal eye fields and shows changes in the spatial profile of its receptive fieldswith attention.V5/MT Visual area V5, V also known as visual area MT (middletemporal), is a region of extrastriate visual cortex that is thought to play a majorrole in the perception of motion, the integration of local motion signals intoglobal percepts and the guidance of some eye movementsMT is connected to a wide array of cortical and subcortical brain areas. Its inputsinclude the visual cortical areas V1, V2, and dorsal V3 (dorsomedial area), thekoniocellular regions of the LGN, and the inferior pulvinar. The pattern ofprojections to MT changes somewhat between the representations of the fovealand peripheral visual fields, with the latter receiving inputs from areas located inthe midline ecortex and retrosplenial ospe regionA standard view is that V1 provides the "most important" input to MT.Nonetheless, several studies have demonstrated that neurons in MT are capableof responding to visual information, often in a direction‐selective manner, evenafter V1 has been destroyed or inactivated. Moreover, research by Semir Zekiand collaborators has suggested that certain types of visual information mayreach MT before it even reaches V1.MT sends its major outputs to areas located in the cortex immediatelysurrounding it, including areas FST, MST and V4t (middle temporal crescent).Other projections of MT target the eye movement‐related areas of the frontaland parietal lobes (frontal eye field and lateral intraparietal area).Function of V5/MTThe first studies of the electrophysiological properties of neurons in MT showed that alarge portion of the cells were tuned to the speed and direction of moving visual stimuliThese results suggested that MT played a significant role in the processing ofvisual motion.Lesion studies have also supported the role of MT in motion perception and eyemovements and neuropsychological studies of a patient who could not see motion, seeingthe world in a series of static "frames" instead, suggested that MT in the primate ishomologous to V5 in the human.However, since neurons in V1 are also tuned to the direction and speed of motion, theseearly results left open the question of precisely what MT could do that V1 could not. Muchwork has been carried out on this region as it appears to integrate local visual motionsignals into the global motion of complex objects ] For example, lesion to the V5 lead todeficits in perceiving motion and processing of complex stimuli. It contains many neuronsselective for the motion of complex visual features (line ends, corners). Microstimulation ofa neuron located in the V5 affects the perception of motion. For example, if one finds aneuron with preference for upward motion, and then we use an electrode to stimulate it,the monkey becomes more likely to report 'upward' motion.There is still much controversy over the exact form of the computations carried out in areaMT and some research suggests that feature motion is in fact already available at lowerlevels of the visual system such as V1MT was shown to be organized in direction columns.NEUROPSYCHIATRY 6010

23/06/54NEUROPSYCHIATRY 61 NEUROPSYCHIATRY 62Organization of V1 and V2.A. Subregions in V1 (area 17)and V2 (area 18). This sectionfrom the occipital lobe of asquirrelmonkey at the border of areas17 and 18 was reacted withcytochrome oxidase. Thecytochromeoxidase stains the blobs in V1and the thick and thin stripesin V2. (Courtesy of M.Livingstone.)B. Connections between V1and V2. The blobs in V1connect primarily to the thinstripes in V2, whilethe interblobs in V1 connect tointerstripes in V2. Layer 4Bprojects to the thick stripes inV2 and tothe middle temporal area(MT). Both thin andinterstripes project to V4.Thick stripes in V2 alsoproject to MT.NEUROPSYCHIATRY 64NEUROPSYCHIATRY 6511

23/06/54Broadmann’ s AreasBroadmann’s area #Brodmann’s area is a region of the cerebral cortex defined based onits cytoarchitectonics, or organization of cellsBrodmann areas were originally defined and numbered by the German neurologistKorbinian Brodmann basedonthecytoarchitecture organisation of neurons heobserved in the cerebral cortex using the Nissl stain. Brodmann published his mapsof cortical areas in humans, monkeys, and other species in 1909, along with manyother findings and observations regarding the general cell types and laminarorganization of the mammalian cortex. (The same Brodmann area number indifferent species does not necessarily indicate homologous areas.)A more detailed and verifiable cortical map have since been published by Constantin vonEconomo and Georg N. Koskinas which greatly improves the quality of the cytoarchitectonicclassifications.Many of the areas Brodmann defined based solely on their neuronal organization have sincebeen correlated closely to diverse cortical functions. For example, Brodmann areas 1, 2 and3aretheprimary somatosensory cortex; area4istheprimary motor cortex; area17istheprimary visual cortex; and areas 41 and 42 correspond closely to primary auditory cortex.Higher order functions of the association cortical areas are also consistently localized to thesame Brodmann areas by neurophysiological, functional imaging, and other methods (e.g.,the consistent localization of Broca's speech and language area to the left Brodmann areas44 and 45). However, functional imaging can only identify the approximate localization ofbrain activations in terms of Brodmann areas since their actual boundaries in any individualbrain requires its histological examination.Brodmann areas for human & non‐human primatesBrodmann’s areas 3Dmap: Lateral Surfacemap: Medial Surface12

23/06/54Brodmann areas for human & non‐human primatesNEUROPSYCHIATRY 75 NEUROPSYCHIATRY 76NEUROPSYCHIATRY 77 NEUROPSYCHIATRY 7813

23/06/54corpus callosum (Latin: tough body), also known as the colossalcommissure, is a wide, flat bundle of neural fibers beneath the cortex in theeutherian brain at the longitudinal fissure. It connects the left and right cerebralhemispheres and facilitates interhemispheric communication. It is the largest whitematter structure in the brain, consisting of 200–250 million contralateral axonalprojections.The posterior portion of the corpus callosum is called the splenium; theanterior iscalled the genu (or "knee"); between the two is the truncus, or "body", of the corpuscallosum. The part between the body and the splenium is often markedly thinnedand thus referred to as the "isthmus". The rostrum is the part of the corpus callosumthat projects posteriorly and inferiorly from the anteriormost genu, as can be seenon the sagittal image of the brain displayed on the right. The rostrum is so named forits resemblance to a bird's beak.Thinner axons in the genu connect the prefrontal cortex between the two halves ofthe brain. Thicker axons in the midbody of the corpus callosum and in the spleniuminterconnect areas of the premotor and supplementary motor regions and motorcortex, with proportionally more corpus dedicated to supplementary motor regions.The posterior body of the corpus communicates somatosensory informationbetween the two halves of the parietal lobe and visual center at the occipital lobeCorpuscallosumCorpuscallosumOccipital lobe lesions• Irritative lesions –seizure– Seizure symptoms: visual hallucinations,consisting of unformed flashes of light andcolors• Destructive lesions– Visual field defects (homonymous field defects)– Psychic blindnessOccipital lobe epilepsy• Seizure symptoms– Visual hallucinations and/or illusions– Blindness or decreased vision– Pallinopsia or image repetition (a visual limage isreplayed again and again)– Sensation of eye movements16

23/06/54Occipital lobe epilepsy• Seizure symptoms (cont.)– Eye pain– Involuntary eye movement to one or other side– Nystagmus or eye jerking to one or other side– Eyelid fluttering• 4 major types of visualfield defects– Altitudinal field defects– Central scotoma– Bitemporal hemianopia– HomonymoushemianopiaVisual field defectsVisual field defectsTypes of visual field defects• Altitudinal field defects = loss of vision aboveor below the horizontal plane• Central scotoma = loss of central vision• Bitemporal hemianopia = loss of vision at thesides• Homonymous hemianopia– Loss at one side in both eyes– Sites of lesion: behind optic chiasmNormalvisual fieldBitemporalhemianopiaPictures from WikipediaTypes of visual field defectsTypes of visual field defectsNormalvisual fieldNormalvisual fieldBinasalhemianopiaPictures from WikipediaLefthomonymoushemianopiaPictures from Wikipedia17

23/06/54Types of visual field defectsNormalvisual fieldRighthomonymoushemianopiaPictures from WikipediaTypes of visual field defectsQuadrantanopia• Contralateral homonymousinferior quadrantanopia =lesion of optic radiation deepin parietal lobe• Contralateral homonymoussuperior quadrantanopia =lesion of optic radiation deepin temporal lobeTypes of visual field defectsMacular sparingPresence of“macular sparing”= occipital lobelesionPicture from www.acbvi.orgOccipital lobe lesions• Damage to areas 18, 19, and 37 (adjacentparietal lobe) – responsible for visualassociation may cause varying degrees ofpsychic blindness– Visual agnosia = inability to recognize objects bysight– Alexia = inability to readAgnosia• The clinical term applied to disorders in whicha patient is unable to attach meaning orsignificance to perceived sensory stimuli(difficulty in identification or recognition)• Visual agnosia = inability to recognize objectsby sightVisual agnosias• Prosopagnosia = the inability to recognizepreviously familiar faces• Visual motion agnosia• Object agnosia = the inability to identify iffamiliar objects by sight• Achromatopsia = visual agnosia limited tocolor perception18

23/06/54Alexia• Alexia = inability to read– Alexia with agraphia• Sites of lesion: parieto‐temporal junction area,particularly the angular gyrus– Alexia without agraphia• Sites of lesion: dominant visual cortex and spleniumof the corpus callosum (posterior cerebral arterylesion)Agraphia = inability to writeThe Occipital Lobes Are the Center of OurVisual Perception SystemThe Peristriate region of the occipital lobe isinvolved in visuospatial processing,discrimination of movement and colordiscrimination.Damage to one side of the occipital lobecauses homonymous loss of vision withexactly the same "field cut" in both eyes.Disorders of the Occipital Lobe Can CauseVisual Hallucinations and IllusionsVisual hallucinations (visual images withno external stimuli) can be caused bylesions to the occipital region or temporallobe seizures.Visual illusions (distorted perceptions)can take the form of objects appearinglarger or smaller than they actually are,objects lacking color or objects havingabnormal coloring.Disorders of the Occipital Lobe Can CauseVisual Hallucinations and IllusionsLesions in the parietal-temporaloccipitalassociation area can causeword blindness with writingimpairments.NEUROPSYCHIATRY 11319

23/06/54Occipital Lobes• A. Area 17• B. Areas 18 and 19A. Area 17NEUROPSYCHIATRY 115NEUROPSYCHIATRY 1161. Deficits associated with lesions-Homonymous hemaniopsia of contralateralvisual field follows unilateral lesion;scotoma, or "blind spot" follows subtotallesion.-Amblyopias, A i areas of intermediate t degree ofchange in visual function, are often foundnear scotomas.-A field defect may be reported as blindnessin the eye on that side.1. Deficits associated with lesions (cont)- Some loss of visual function may occur inintact half fields in homonymoushemianopsia.- Central scotomas may lead to subjectivelynormal visual fields with reduced acuity.- Macular sparing may occur if the lesion isclose to the occipital pole.NEUROPSYCHIATRY 117NEUROPSYCHIATRY 1181. Deficits associated with lesions (cont)Bilateral ablation may result in "corticalblindness" (inability to see, with denial andconfabulation, sometimes called Anton'ssyndrome) or to subtotal blindness withresidual ability to discri- minate luminousflux and a speckled from a grey field.1. Deficits associated with lesions (cont)- Interruption of optic pathways mayproduce similar, but not always identicalsymptoms to lesions of area 17.-Acute trauma may cause warping ofvisual coordinates, distortions, andpolyopias. These symptoms maydisappear within days or last for months.They may reap-pear ictally.NEUROPSYCHIATRY 119NEUROPSYCHIATRY 12020

23/06/541. Deficits associated with lesions (cont)-Toxic states may produce transitions fromvisual distortion to blindness and backagain.- Eye movement may be affected differen-tially by right or left occipital lesions; leftlesions will shift to compensate for ascotoma while right lesions may not followin the area of the scotoma.1. Deficits associated with lesions(cont)- Left occipital lesions with involvementof the splenium of the corpus callosummay result in alexia without agraphia.- Focal seizures consisting of visualsensations have been associated withlesions found in area 17.NEUROPSYCHIATRY 121NEUROPSYCHIATRY 122NEUROPSYCHIATRY 123 NEUROPSYCHIATRY 1242. Tests for dysfunction-Perimetry allows definition of limits ofscotoma. Harms perimeter allowsdefinition in terms of contour, spectralvalues, intensity , as well as critical flickerfrequency.-Amblyopias may also be tested with Harmsperimeter; deficits are found in criticalflicker frequency, dark adaptation, and twopoint resolution.2. Tests for dysfunction (cont)-Homonymous hemianopsia indicates corticallesion or interruption of optic radiations, whilebitemporal hemianopsia indicates interruptionof the optic pathway at the optic chiasm.-Monocular blindness results from unilateraldestruction peripheral to the chiasm, andquadrantonopsia from selective interruption ofthe radiation fibers in one hemisphere, eithertemporal or nasal but not both.NEUROPSYCHIATRY 125NEUROPSYCHIATRY 12621

23/06/542. Tests for dysfunction (cont)-Macular sparing indicates that the lesioninvolves the occipital cortex, rather than theoptic radiations. Occlusion of the posteriorcerebral artery should be suspected.-"Filling in" of a scotoma may be tested bypresentation of a horizontal line crossing thevisual field with a gap in the scotomatousarea. Patients report seeing a completed lineif filling in occurs.NEUROPSYCHIATRY 1272. Tests for dysfunction (cont)- Eye movement can be tested by having thepatient follow a moving target.- Occipital lobe and posterior occulomotorlesion patients can do this; frontal lobe oranterior ocularmotor lesion patients cannotfollow the verbal command with voluntaryfollowing.- Right occipital lesions will not follow intothe left half field.NEUROPSYCHIATRY 1282. Tests for dysfunction (cont)Forced choice (guessing) discriminationof a stimulus may result in identificationof objects within a scotoma, although ifasked to identify a stimulus the patientreports he does not see it.B. Areas 18 and 19NEUROPSYCHIATRY 129NEUROPSYCHIATRY 130Tests for dysfunction-Sensory deficits such as rapid visual fatigue,impaired visual adaptation, and raised visualthresholds indicate involvement of 18 or 19.-Visual l following is tested by looking foropticokinetic nystagmus generated byfollowing moving vertical black lines on awhite background.Tests for dysfunction (cont)Unilateral spatial agnosia is tested bypicture copying (details on the left may beomitted) or card sorting (cards on the left areignored).NEUROPSYCHIATRY 131NEUROPSYCHIATRY 13222

23/06/54Tests for dysfunction (cont)Tests for degree of bilateral deficit may bedone in order from simplest to mostcomplex: identification of clearly drawnpictures, identification of complex orindistinct tpictures, it identification ofscribbled-on pictures, identification ofhidden structures or Raven's ProgressiveMatrices Test.C. Types of Visual AgnosiasNEUROPSYCHIATRY 133NEUROPSYCHIATRY 134Visual agnosiaAn associative visual deficit in whichperception and acuity are relativelynormal, while the recogni- tion andmeaning of the percept are absentVisual object agnosiaA deficit in which visual perception isintact, but recognition and ascription ofmeaning to objects seen is impaired.This defect is associated with a rightoccipitoparietal lesion although similarleft hemisphere lesions are frequentlypresent.NEUROPSYCHIATRY 135NEUROPSYCHIATRY 136Visual object agnosia (cont)Test -- naming of simple objects andpictures, naming of complex or ambiguouspictures, locating visual stimuliwith interference or with picturessuperimposed on each other, fragmentedletters, the Benton Visual Retention Test,and WAIS Object Assembly.ProsopagnosiaThe inability to recognize familiar faces.This is a special type of visual object agnosiaand often occurs with other visual agnosias.It is most frequently seen with rightoccipitoparietal and occipitotemporallesions.Test -- matching of facial pictures andidentification of famous faces.NEUROPSYCHIATRY 137NEUROPSYCHIATRY 13823

23/06/54Color agnosiaA defect of color recognition which has avariety of forms, primarily an inability toname or discriminate between colors.The color name may be given in a qualified orconcrete form or a confabulation may occur.It sometimes accompanies alexia and aphasia.Usually results from a left occipital or occipitotemporallesion.Color agnosia (cont)It sometimes accompanies alexia andaphasia.Usually results from a left occipital oroccipitotemporal p lesion.NEUROPSYCHIATRY 139NEUROPSYCHIATRY 140Color agnosia (cont)Test:Matching names to colors and colorsto names, color sorting, arrangingshades of a color by intensity, coloringpictures appropriately,identificationof inappropriatelycolored objects.SimultanagnosiaThe inability to absorb more than one objector aspect of a visual stimulus at a time.This condition occurs with bilateral lesionsof the occipitoparietal region.When accompanied by incoordination ofocular movements, this defect is known asBalint's syndrome.NEUROPSYCHIATRY 141NEUROPSYCHIATRY 142Simultanagnosia (cont)TestHave patient attempt to draw a linearound shapes (circle, square,triangle),or write with eyes open, thenclosed (with Balint's syndrome, closingeyes improves handwriting)MetamorphopsiaObjects are correctly recognized but aresubjectively distorted.Lesions of the occipital lobe produce simplerdeficits, while parietal lesions tend toproduce intermediate effects, , and temporallesions are associated with more complexdisorders.Teleopsia objects appear small and at adistance.NEUROPSYCHIATRY 143NEUROPSYCHIATRY 14424

23/06/54Metamorphopsia (cont)Teleopsia objects appear small and at adistancePelopsia objects appear to loom up close.Loss of stereoscopic vision.Palinopsia (paliopsia) -- perseveratoryillusions which are superimposed uponobjects currently in the visual field. Thisdefect usually occurs in the presence of aright occipitotemporal lesion.Metamorphopsia (cont)TestAssess qualitative visual changes viapatient report and tasks tapping visualdisorientation, i ti inattention, ti fluctuation,tidelayed recognition of forms, imperfectsynthesis of moving objects, and alteredrate of flicker-fusion.NEUROPSYCHIATRY 145NEUROPSYCHIATRY 146D. Integrative FunctionNEUROPSYCHIATRY 147NEUROPSYCHIATRY 148OpticKinesthetic motor organization. Sincemovement entails a number of systems, itis necessary to check all components of themovement function in assessing a dfiit deficitIntegrity of the visual-spatial basis ofmovement.Impairment of this component is due to alesionin the inferior parietal and/orparietoccipital region, especially on theright.Test -- have patient reproduce theexaminer's hand and pencil movementswith examiner sitting beside, thenopposite, the patientNEUROPSYCHIATRY 149NEUROPSYCHIATRY 15025

23/06/54Integrity of the kinesthetic basisof movement.Impairment of this component, orafferent apraxia, is usually due to alesion in the post-central gyruscontralateral to the impaired sideof the body.Movements tend to be awkward ordiffuse in character.Integrity of the kinesthetic basisof movement (cont).TestCheck basic sensory adequacy;then witheyes closed place patient's hand in oneposition and ask him to reproduce theposition with the other hand; ask patient toreproduce position of examiner's hands orfollow verbal commands for hand positionwithout looking at his own.NEUROPSYCHIATRY 151NEUROPSYCHIATRY 152Integrity of motor or dynamic basisof movement.Impairment of this component, or efferent apraxiais due to lesions of the premotor area, especiallyin the dominant hemisphere. It results inperseverative movements and the loss ofcontinuity i of movement.Test -- tasks requiring reciprocal coordination ofboth hands, alternating tapping patterns, ring-fisttest, fist-edge-palm test, and drawing ofalternating designsWord fluencyHas come to be associated with the leftfrontal area due to its disturbance withlesions in this region. It is hypothesizedthat the left hemisphere is necessary forverbal facility and the frontal area for theability to switch sets.Test -- have patient write or say as manywords as possible that begin with a givenletter in a given time period .NEUROPSYCHIATRY 153NEUROPSYCHIATRY 154Severe memory deficitsHave been reported with bilateral temporallesions and these have been thought to bedue to hippocampal damage.However, recently damage to temporal stemhas been postulated to produce severelearning and retention deficits in thepresence of intact hippocampi.Severe memory deficitsTest -- memory for verbal story, hiddenobjects, design reproduction frommemory, paired associates, andmemory for four unrelated wordsafter interference.NEUROPSYCHIATRY 155NEUROPSYCHIATRY 15626

23/06/54Callosal DisconnectionSyndromesNEUROPSYCHIATRY 157NEUROPSYCHIATRY 158NEUROPSYCHIATRY 159 NEUROPSYCHIATRY 160NEUROPSYCHIATRY 161 NEUROPSYCHIATRY 16227

23/06/54NEUROPSYCHIATRY 163การเล่นของเล่นที ่เหมาะสมกับวัย ช่วยส่งเสริมพัฒนาการของสมองและการเรียนรู ้28