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Anatomical studies in lobotomy Smythies, John Raymond 1955

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i ANATOMICAL STUDIES IN LOBOTOMY by JOHN. RAYMOND SMITHIES A"THESIS SUBMITTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF in the Department of Neurological Research We accept this thesis as conforming to the standard required from candidates for the degree of MASTER OF SCIENCE Members of the Department of AfeuW<^««/ &4£4#etd THE UNIVERSITY OF BRITISH COLUMBIA March, 1955 ABSTRACT This thesis contains a report of an investigation that has been carried out over the l a s t year and a half into the tracing of fibre tracts i n the human brain by the method of terminal degeneration. Four brains have been used and the extent of the degeneration (where present) i n each has been traced i n d e t a i l . Particular attention has been paid to improving the method of terminal degeneration by setting up and using objective and quantitative c r i t e r i a of degeneration i n place of the subjective and qualitative c r i t e r i a that have been used i n the past. Descriptions of the different appearance of degeneration i n different parts' of the nervous system are also given. Thus an accurate account can be given of the fibres cut i n these cases of prefrontal lobotomy and of the efferent projections of that part of the frontal lobe undercut by the lesion. These accounts help i n placing the operation on a rational basis and give information on the anatomy of the connexions i n the human brain that cannot be obtained i n any other manner. ACKNOVJLEDGEMENTS I am most grateful to Professor W. C. Gibson for his direction and advice during this work supervised by him. I should also like to record my gratitude to Mrs* Nan Purkis and Hrs. Linnea Lowes for their technical assistance in preparing some of the sections and photographs and for examining some of the cortical sections; to Mrs. Nan Cheney who prepared the artist's drawings from originals prepared by myself; to Miss Susan Calthrop who typed the thesis and to Professor Paul Yakovlev and Brigadier Elbert DaCoursey for the presentation of the pathological specimens. i i i TABLE OF CONTENTS CHAPTER PAGE I. INTRODUCTION AND SURVEY OF PREVIOUS LITERATURE , 1 II. MATERIAL AND METHODS . . .• 13 III. RESULTS 19 :-TV. DISCUSSION .' 24 V. SUMMARY 27 BIBLIOGRAPHY 28 iv DESCRIPTION OF FIGURES MAPS 1 - 3 Maps of lobotomy wound: brain L-2 (R) 4 - 6 The same: brain L-2 (L) 7 - 9 The same.: brain L-3 (R) 10 - 13 The same: brain L-4 •....) 14-19 Extent of the degeneration in the dorso-medial nucleus of the thalamus of brain L-2 (R) 20 - 23 The same : brain L-2 (L) 24 - 30 The same : brain L-3 (R) (Note figure 26 is from a section as shown in figure 25 in which the presence of any bouton or terminal was marked on the map with a dot.) 31-34 The same : brain L-4 (R) 35-41 Extent of degeneration in the prefronto-pontine tract and pons of brain L-3 (R) 42 - 46 The same : brain L-4 (R) In figures 42 - 43 one stroke stands for 2 fields. 47 - 49 Extent of the degeneration in the medial mamillary nucleus of brain L-4 (R) 50 Extent of 'degeneration1 in the normal pons (NC2) mapped by 'dorso-medial' criteria. Mapped by 'pons' criteria this map. would be blank. 51 The same for the nucleus parafascicularis CAMERA LUCIDA DRAWINGS 52 - 55 Drawings of degenerating terminals in the dorso-medial nucleus-Units of degeneration are numbered. REPRODUCTIONS 56 From Hoff ('32 a) 57 From Hoff ('35) 58 From Brodal ('49) 59 From Brodal, Walberg and Blackstad ('50) 60 From Getz (»52) 61 From Meyer ('49) PHOTOMICROGRAPHS 62 - 63 Degeneration immediately around the lesion i n brain L-2. x 1,400 64 Degeneration i n the dorso-medial nucleus i n brain L-2. x 1,700 65 The same i n brain L - 4 . x 900 66 Normal boutons termineaux i n nucleus parafascicularis (NCl). x 1,600 67 The same. x 1,400 68 Degenerating fibres i n the prefronto-pontine tract i n brain L - 3 . x 1,800 69 The fibre plexus i n the normal pons (NC2). x 1,100 70 Degeneration i n the pons i n brain L-4« x 1,000 71 70 enlarged, x 1,800 72 - 73 The fibre plexus i n the normal medial mamillary nucleus (NCl) x 1,100 74 Degeneration i n the medial mamillary nucleus of brain L-4» x 1,100 v i ABBREVIATIONS USED IN FIGURES FIGURE 1 - 1 3 a agranular e . eulaminate d dys granular m mesocortex 1 4 - 4 9 A.C. anterior commissure A.D. , antero-dorsal nucleus A.H. anterior hypothalamus A.L. ansa lenticularis A.M. antero-medial nucleus ATR. anterior thalamic radiation CM. nucleus centralis medialis C. N. caudate nucleus CE.N. nucleus centranum medianum D. H. dorsal hypothalamus D.L. dorso-lateral nucleus D.M. dorso-medial nucleus F. fornix F. L. fasciculus lenticularis G. P. globus pallidus I.C. internal capsule I.T.P. inferior thalamic peduncle L.H. l a t e r a l hypothalamus L.M. la t e r a l mamillary nucleus L.T.(Tu) l a t e r a l tuberal nucleus mc large-celled portion M.B.(M) mamillary body M.L. medial leminiscus v i i FIGURE M.T. mamillary-thalamic tract N.A. anterior nucleus N.S.M. supra-mamillary nucleus N.V. ventral nucleus pc small-celled portion P. pyramidal tract P.F. parafascicular nucleus F.H. posterior hypothalamus P.T. parataenial nucleus PU. pulvinar PUT. putamen E.V. paraventricular nucleus Pa.Cd. dorsal part of paracentral nucleus Pa.Cv. ventral part of paracentral nucleus R. red nucleus R.E# nucleus reuniens S.N. substantia nigra S.T. subthalamus SUM. nucleus submedius Th. thalamus V.A. anterior ventral nucleus V.L. l a t e r a l ventral nucleus V.P. posterior ventral nucleus Z.I. zona incerta 52-55 g. g l i a l c e l l N. nerve c e l l c• capillary v i i i SIGNS USED IN FIGURES THALAMUS HYPOTHALAMUS PONS (except 41, 50) FIGURES 41, 50 • 2 - 1 4 units of degeneration. 4- more than 14 units of degeneration. • 2 or more units of degeneration plus obvious fragmentation of the fine, plexus of unmyelinated f i b r e s . • more than 50 boutons and terminals plus obvious fragmentation of the fine plexus of myelinated f i b r e s . more than 15 boutons. c 2 units of degeneration. • both. In a l l cases the sign ^  shows the presence and approximate direction of degenerated fibres i f more than 1 present. CHAPTER I INTRODUCTION'AND SURVEY OF PREVIOUS LITERATURE The method of terminal degeneration used to trace neuronal connexions i n the nervous system depends on the fact that, following the cutting of an axon, the axon, i t s preterminal branches and the terminals themselves undergo a series of characteristic changes that can be detected by the use of s i l v e r stains* The f i r s t account of terminal degeneration i n the axon was given by Nikolajew (1893)• He' used the methylene blue method to show the degenerating boutons on the ganglion'cells of the frog's heart ten to fifteen days after cutting the vagus nerve. The normally delicate ring endings became fragmented and hypertrophied. Tuckett (1895) used the same technique to demonstrate degenerating pre-ganglionic fibres i n the rabbit. Cajal (*ll) makes the important point (in addition to others) that where an axon i s interrupted i n the white matter i t s central segment forms a late 'boute de retraction', having passed through a complex and slow hypertrophy with fusiform swellings, varicosities and 'boute en series'. The peripheral, or severed part of the axon passes through active phases of neurofibrillar swelling, formation of isolated spheres, and complicated clusters of neurofibrils showing that l o c a l reaction i s possible even i n the isolated portion. Ranson and Billingsley ('18) using a pyridine s i l v e r method were unable to demonstrate the normally dense plexus of fibres i n the superior cervical ganglion following the section and subsequent degeneration of the pre-ganglionic trunk. The History of the Method* (a) The early years* De Castro ('30) carried out an intensive investigation into the degeneration i n the superior cervical ganglion i n over 100 cats (chiefly young). He used block s i l v e r impregnation methods with fixation i n somnifene or chloral hydrate and showed that terminal degeneration appears at the end of seventeen hours although the axons to which they were attached were often intact. This work was confirmed by Lawrentjew (*34) who used the method of terminal degeneration to determine the method of ending of fibres i n the superior sympathetic ganglion. At about the same time Levi ('32) studied degeneration i n nerve processes separated from their c e l l bodies i n tissue culture. Twelve hours following section the d i s t a l segment resembled a 'string of pearls', the swellings of which were in the process of fragmentary degeneration. Sereni and Young ('32) detected bouton changes i n cephalopods fi f t e e n hours after the mantle connective and s t e l l a r nerves had been sectioned and the process was complete i n 7 days with gradual disappearance of fragments. (b) Recent work. The recent use of the method dates from Hoff*s series of investigations. In these he examined the degeneration produced i n the cat spinal cord (r32a) after cutting the afferent roots of post-thoracic nerves. He then used the method (*32b, '35) to study the termination i n the cord of fibres from the motor and premotor cortex i n the cat and monkey. Gibson ('37) described the changes i n the terminals In the spinal cord following i t s transection i n the cat. Schimert ('38) used the method to trace the endings of the vestibulo-3 spinal tract i n the cat. This was followed by a number of communications from Glees and Le Gros Clark ('41) and Glees (*41, '42) i n which the mode of temmination of the optic nerve i n the lat e r a l geniculate body i n various animals was studied* Glees ('44) studied cortico-striate connexions i n cats* Glees, Meyer,and Meyer ('46) used the method to trace the terminal degeneration i n the frontal cortex of the rabbit following interruption of afferent fibres, and Le Gros Clark and Meyer ('47) used i t to -trace the terminal connexions" of the olfactory tract i n the rabbit. Brodal ('49) and Brodal, Walberg and Blackstad ('50) investigated the termination of the spinal afferents In the l a t e r a l reticular nucleus of the cat and the termination of the spino-olivary fibres respectively. Adey ('51) and Getz ('52) used the method to trace the hippocampal connexions of the cingulate cortex of the rabbit, and the termination of spino-thalamic fibres i n the cat respectively. I t has been applied to human lobotomy material by Meyer ('49), Beck, Meyer and Le Beau ('51) and Martinez ( f55)* We w i l l now consider, the question - How can this method be used so as to give as accurate and consistent results as possible? Three elements i n the answer to this question can be isolated* (1) A method of silver staining that w i l l give reasonably consistent results must be used* (2) The c r i t e r i a which are used to decide i f a given region contains degeneration should be made as objective as possible* (3) The method of presenting the results should be as accurate as these c r i t e r i a allow. To take these i n turns (1) We have found that Gibson's modification of Rio-^Hortega's double-impregnation technique gives the consistent results providing that certain precautions are taken. We have described the method i n detail elsewhere ( 155)• The main points are that the material must be properly fixed and that the pH and temperature of the s i l v e r solutions must be kept within narrow l i m i t s . (2) In a l l previous investigations the c r i t e r i a of deggaaeration have been qualitative and subjective. Decisions as to whether degneration i s , or i s not, present have been made on the basis of subjective comparisons with sections taken from the same region of a normal brain. These subjective c r i t e r i a of degeneration are similar for most workers. The f i e l d must contain large argentophile masses, either s o l i d or thick-ringed, usually of irregular shape and (in later cases) fragmenting. The more regular of these are regarded as being degenerating boutons termineaux and the more irregular, particularly i f i n visible continuity with a degenerating fibre, are regarded as being degenerating pre-terminal fi b r e s . The two are subsumed under one term - degenerating 'terminals'. The presence of degenerating fibres i n the f i e l d has been regarded as more reliable evidence that degeneration has taken place i n that f i e l d . As degeneration proceeds a progression from normal looped boutons to thickened, solid, and l a s t l y fragmented boutons has been described (Hoff «32 a and b, Gibson '37, and others). Hoff ('32a) recognized a thickening (or f i l l i n g in) of the ring form of the bouton, swelling, granularity, irregularity of shape (often pear-shaped or great elongation) and a darkness of staining as evidence of degeneration* Hoff (f35) mentions only 'Progressive swelling and granulation 1 followed by 'an early disintegration' as signs of degenerating bouton termineaux* Gibson ('37) summarised the process of degeneration as follows: an average degenerating bouton passes through the processes of hypertrophy, elongation, fragmentation and granulation, and from the circular to the .•' e l l i p s o i d and back to the circular again.' Fedorow and Matwejewa ('35) described the following succession of changes i n the degeneration of terminals i n the frog: Stage 1. Increased argentophilia of fibres and boutons* Stage 2. Swelling of fibres and boutons. Stage 3*. Varicosities appear on the f i b r e s . Stage 4-* Vacuolation appears i n the boutons* This stage i s reached in the autumn i n 11-12 days and i n the winter not u n t i l 25-30 days. Stage 5* Disintegration* Glees and Le Gros Clark ('41) recognised swelling, thickening or a f i l l i n g i n of the ring (often with a dense, opaque mass composed of a very fine neurofibrillar ruetwork) and increased argentophilia as evidence of degeneration. They noted that there was considerable variation i n the extent of degeneration, some terminal remaining quite small. Swollen, argentophilic fibres (particularly at their sites of branching into the terminal divisions) with 'cylindrical' swellings i n their course were regarded as being degenerating* Glees ('4-1) noted that the normal terminal rings (present i n great numbers i n the l a t e r a l geniculate body of the cat) had mostly been transformed into thicker rings or into s o l i d black bulbs which later disintegrated into small granules. 'In addition there are also to be seen oval or elongated end-formations i n the substance of which a strongly staining neurofibrillar network i s v i s i b l e . ' Glees ('42) described similar changes i n the rabbit and i n the caudate nucleus of the cat ('44) the degenerating fine terminal fibres were swollen (particularly where the main fibre broke up into i t s terminal branches) and fragmented. Terminal arborisations had a fine beaded appearance. Glees, Meyer and Meyer ('46) noted the following signs of degeneration at the termination of injured axons/ a thickening (or f i l l i n g in) of the rings and the presence of f i b r i l l a t e d ring structures.and a beading and granular disintegration of fine fibres followed by a distinct rarefaction of fine fibre plexus i n the cortex. In the course of the fibres they recognised a progressive swelling, ballooning and fragmentation of thicker f i b r e s . Le Gros Clark and Meyer ('47) used rigorous but s t i l l subjective c r i t e r i a of degneration. They compared the region under examination f i r s t with the unoperated side of the same animal and also with the same region of an entirely normal rabbit's brain 'which had been fixed and stained under exactly the same conditions as the operated cases'. Their c r i t e r i a of significant degeneration were 'a massive degeneration of terminals, preterminals or unmyelinated fibres' followed i n other experiments after a longer time interval by an actual loss of fibres i n the same region. They considered that the massive degeneration, when found, provided conclusive evidence of terminal connexions but that i t s absence did not mean that no interrupted fibres terminated i n the region. 7 Brodal (f4-9) described degenerating boutons as 'more or less spherical, ovoid or more irregular, sometimes almost triangular 1 1 enlarged and argentophilic, sometimes with a lighter center* The degenerating fine fibres appeared as 'threads varying extremely i n caliber along their course, swollen globular,' spindle-shaped or ovoid parts being inter-connected with attenuated fragments of the original f i b e r ' • These showed vacuolisation and later fragmentation* Brodal notes that Phalen and Davenport ( '37), Barnard ( '40) , Minckler (*U0) and others had claimed that the appearance of normal terminal boutons may vary considerably and that 'pictures closely resembling degenerated boutons may quite frequently be seen 1• He therefore took no. account of 'Scattered structures with the morphological characteristics of degenerating boutons,' but only of 'larger quantities 1 of them* He l a i d more emphasis on 'the occurrence of fine degenerated terminal and preterminal fibers than on degenerated boutons' and (as 'additional evidence') the 'very clear cut loss of the fine fibers which can be seen after 7 days or more • • •'. Blackstad, Brodal and Walberg ('51) make a further analysis of the method pointing out that 'The vagaries of the si l v e r techniques are well-known' and that ' A l l authors studying normal terminal boutons agree that they are frequently d i f f i c u l t to identify.' They also note that there i s not general agreement as to what i s , and what i s not, a degenerating bouton. They bring to notice one very important fact, namely that the picture of terminal degeneration i s not the same everywhere. A particular feature of their findings was, i n some areas of the olive, a great increase i n the number of stained boutons (from an average of 3 to as many as 25 per f i e l d ) and an increase i n the 8 proportion of large and so l i d boutons and those of irregular shape* Whereas i n other regions of the olive 'where pronounced alterations of fine nerve fibres are evidence of marked terminal degeneration the number of boutons appears not to be raised*' They conclude 'Only when the increase of boutons i s exceptionally high i n experimental animals can an area of degeneration be determined on this basis exclusively* jfhis i s the f i r s t time that we have come across the suggestion that the mere increase i n the number of boutons visible may be used as an exclusive criterion of degenerationjj In most instances the concomitant degeneration of the finest fibres i s a more reliable sign* An increased number of solid, degenerating boutons i s , however, significant enough of terminal degeneration to be of practical value•* The d i f f i c u l t i e s here are (i) how large must the increase i n numbers be before i t can be considered significant, and ( i i ) even within one nucleus there may be great differences of bouton concentration and morphology and so i t i s not sufficient to compare the degenerated with the normal unless both the extent of the variation of the boutons i n different parts of one nucleus and i n the same parts of the same nucleus i n different brains i s known i n much more detail than i t i s at .present* However, i t must be noted that these same authors ('50) had previously only accepted the presence of degenerated fine fibers as c r i t e r i a of degeneration* Wall, Glees and Pulton ('51) stated that i n view of 'the d i f f i c u l t i e s involved i n the fine-fibre staining technique, we have recognised degeneration as occurring only i n the following circumstancess f i r s t , when there was clear contrast between the operated and control sides stained simultaneously; second, when the section showed a clear agranular background with discrete parallel-sided fibres; third, only gross distortions of fibre shape and termination were accepted as evidence of degeneration* 1 Adey ( f5l) does not give his c r i t e r i a of degeneration except to say that degenerating terminals are 'swollen 1* Getz ('52) states that 'provided that a comparison with normal material i s carefully carried out and that also degenerated terminal fibres are found - the differences between the normal and the degenerating structures are sufficiently clearcut to allow an exact mapping out of the termination of transected fibre tracts•' His c r i t e r i a for the degeneration of boutons are - an increase i n number of a l l types, especially of solid black boutons, 'the shape of several boutons being oval and irregular*' He states, however, that the.finding of degenerated boutons alone i s not sufficient to allow the diagnosis of terminal degeneration '*•• this diagnosis can only be made when degenerating terminal fibres are also present'• His c r i t e r i a of the degeneration of terminal fibres are a 'drop-like appearance ••• "beading vacuolisation and an increased a f f i n i t y for s i l v e r . ' He would not include fibres distinguished only by'irregular contours and diameters'* Notice that Getz would only recognise degenerating fibres as providing certain evidence of degeneration whereas Brodal, Walberg and Blackstad would also recognise an 'exceptional' increase i n the number of boutons or 'an increased number of solid, degenerating boutons1 as well* Glees and Le Gros Clark ('41) quote Schimert ('38)* '.JHe] considers that the appearance of the end-bulb i t s e l f i s not always a safe criterion of degeneration, unless i t i s accompanied by degenerative changes affecting 10 the terminal f i b r e which c a r r i e s i t . ' However, i t i s not always obvious whether a given structure i s a degenerating bouton or terminal f i b r e * Meyer ('4-9), using human lobotomy material, followed these c r i t e r i a o f degeneration 'gross changes o f axons and terminals'; i n the case of boutons the r i n g form had to be completely f i l l e d i n and replaced by 'large homogeneous or d i s i n t e g r a t i n g swellings'}, i n the case of preterminal f i b r e s these had to be 'broken up i n t o f i n e droplets'} f i b r e s had to show 'fragmentation and v a c u o l i s a t i o n together with a marked swelling •*• i n t h e i r course.' Beck, Meyer and LeBeau (*5l) recognised only 'an accumulation of gro s s l y degenerated f i b r e s and/or terminals 'as s i g n i f i c a n t of degeneration. They stated furthermore tha t 'Negative fin d i n g s i n a given area could s a f e l y be regarded as proof o f the absence of any f i b r e connexion with the ablated or i s o l a t e d region.' (our i t a l i c s } ; see a l s o Le Gros Clark and Meyer ('4-7) on-this p o i n t ) . Martinez (*55) recognises 'hyperargyrophilic' f i b r e s and 'hypertrophic' boutons or 'club-shaped' terminals as being degenerated. (Note however that i n our opinion the boutons shown i n h i s f i g u r e s 6 and 8 could w e l l be normal f o r the globus p a l l i d u s and the pons.) I t w i l l be noticed that i n a l l the accounts given above the c r i t e r i a of degeneration have been q u a l i t a t i v e and subjective and moreover have d i f f e r e d somewhat from worker to worker (owing, probably to some extent, to the d i f f e r e n t regions and d i f f e r e n t species examined and to the d i f f e r e n t stains used). I t w i l l be c l e a r that consistent and comparable r e s u l t s may not be obtained i f d i f f e r e n t c r i t e r i a are used by d i f f e r e n t people. (3) The method of presentation of the r e s u l t s . In the case of nearly a l l workers the evaluation of the extent of the degeneration has been presented ( i ) by written reports; ( i i ) by means of freehand drawings, or drawings made by some kind of projection apparatus, on which the extent of the degeneration i s marked by dots, cross-hatching, et c * inserted by freehand (for examples see figures 58-61); and ( i i i ) by photomicrographs* In Hoff's f i r s t presentation (>32a), however, dots were used on a camera lu c i d a drawing of the cord to show the loca t i o n of a c e l l supporting degenerating boutons ( f i g . 56). In his next presentation ('32b) round black dots were used to show the position.of each c e l l supporting degenerating boutons, and black triangles showed the position of dendrites supporting degenerating boutons• Crosses were used to show the pos i t i o n of peri d e n d r i t i c degenerated boutons occurring very close to the c e l l body. In his 1935 paper the method was the same but no crosses were used ( f i g . 57). I t therefore seemed to us that, i n order to make t h i s method more rigorous, more objective c r i t e r i a of degeneration should be attempted and more precise methods of presenting the extent of degeneration hasevolved. The subjective and qua l i t a t i v e evaluation of degeneration has given reasonably accurate re s u l t s i n the hands of experienced workers but there i s always the danger that not a l l the p o t e n t i a l l y available information w i l l be gained from the inves t i g a t i o n . That i s to say that f i n e r d e t a i l s of d i s t r i b u t i o n of severed f i b r e s may be l o s t that might have been revealed by objective and quantitative scanning methods* Furthermore, using the l a t t e r methods, the resu l t s of d i f f e r e n t workers could be compared with more precison than could be attained when the c r i t e r i a that each worker uses d i f f e r from those used by other workers to a greater or lesser extent. However, to be of much use, these c r i t e r i a would have to obtain general acceptance as i t would be of l i t t l e advantage i f every worker set up his own objective c r i t e r i a of degeneration. CHAPTER II MATERIAL AND METHODS Four lobotomised human brains were available for this study. L - l . This brain came from a case with a survival time of only five days and no signs of degeneration were found (except immediately around the wound) i n spite of intensive search. L-2. This brain was obtained from a case of bronchogenic carcinoma who died aged 4-9 at the time of death. A bi l a t e r a l prefrontal lobotomy was performed for intractable pain on A p r i l 11th, 1950. The day following the operation the patient was alert but had nausea and was incontinent. Four days after the operation he became dyspneic and irr a t i o n a l and he died on the seventh post-operative day. On examining the right side of the brain a leucotome entry mark could be seen on the extreme la t e r a l edge of the orbital surface of the frontal lobe at the posterior end of the inferior frontal gyrus. Coronal sections of the frontal lobe are shown i n figures 1-3* The lesion extended upwards and forwards undercutting the eulaminate cortex of the l a t e r a l surface of the frontal lobe. Nissl stained sections showed that the region of entry lay just anterior and l a t e r a l to dysgranular cortex. On the l e f t the leucotome had entered a l i t t l e farther forward i n the posterio-intermediate part of the middle frontal gyrus.' . Nissl stained sections showed that this was anterior to dysgranular cortex. The lesion extended forwards and upwards as on the right side (figs • 4.-6) • L-3. This brain was obtained from a case of schizophrenia (paranoid type) 25 years old at the time of death. On November 6th, 194-7 b i l a t e r a l prefrontal lobotomy was performed. Four days later he developed a temperature and a wound infection was noticed. Meningitis developed. Seven days after the operation the patient died following four generalised epileptiform convulsions. On examination of the right side of the brain the entry of the leucotome was visible i n the middle of the middle frontal gyrus i n Brodmann's area 9* Nissl sections showed this to be anterior to dysgranular cortex. The lesion extended downward and backwards to enter the anterior pole of the corpus striatum (figs• 7-9) • The lesion on the l e f t side was essentially similar. 1 L-4. This brain was obtained from a case of schizophrenia (hebephrenic type) aged 43 at the time of death. Bilateral prefrontal lobotomy was performed on August 17th, 1948 described as 'cortical undercutting of areas 9 and 10.' Twelve days after the operation the patient suddenly collapsed and a spinal puncture revealed a pressure of 500 mm. of water. An exploratory operation revealed extreme oedema of the brain. On each side of the brain the entry mark of the leucotome was visible i n the middle of the superior frontal gyrus on the dorsal convexity i n front of the dysgranular cortex (confirmed by Nissl staining). The lesion extended downward and forward to the extreme frontal pole. On the right side the leucotome had penetrated the cortex again to emerge from the brain through the frontal pole. On both sides the upper half of the prefrontal region had been undercut including some damage to the cortex of the cingulate region. There were also signs of recent haemorrhage i n the anterior part of the corpus callosum. Although the leucotome entered eulaminate cortex and i t s path had extended forwards, 15 there vas also brain damage (haemorrhage, softening and discolouration) extending backwards so as to cut into the ro s t r a l t i p of agranular cortex (figs. 10-13). Each brain arrived fixed i n formalin and sectioned by the pathologist conducting the post-mortem examination. Drawings of each brain and each s l i c e of brain were made from different aspects. Sections from the frontal lobe cortex were cut on a freezing microtome at 20 u followed by sections taken to include the thalamus, hypothalamus and related structures; the red nucleus, substantia nigra and related structures; the basal ganglia and internal capsule; the hippocampus and amygdala; and the pons. These sections were stained by Gibson's modification of Rio-Hortega's double impregnation method. At a pH of 10.6 this stain also provides a good method of determing cytoarchitectonic features since, at this pH, the c e l l bodies are stained d i f f e r e n t i a l l y with respect to the background. We have used this as a 'Nissl' stain as well as Cresyl v i o l e t . In the locations where degeneration was found accurate maps were prepared by plotting the outline of the nuclei on graph paper from readings taken from the micrometer scale of the moving stage of the microscope. The presence and extent of degeneration were inserted as follows : (l) Objective c r i t e r i a of degeneration were set up. These c r i t e r i a were chosen after studying a large number of sections from these brains (not L-4 which we did not receive u n t i l much later than the other three) together with sections of the same part taken from each of our three normal control brains (NCI, NC2, and NC3; see Smythies, Gibson and Purkis '55). In the case of the dorsomedial nucleus of the thalamus the following c r i t e r i a were decided upon? (i) One unit of degeneration was defined as a dark purple"*- object i n the f i e l d larger than 2.5 u i n average diameter; either s o l i d or, i f perforated, the diameter of the hole (or holes) was not to exceed l/3 of the total diameter of the object; and possessing an homogeneous internal structure (studies of brains with longer survival times than ours would presumably have to allow for the f i n a l stage of fragmentation)* I f there were two units of degeneration i n a f i e l d (using a x 100 objective and a x 8 ocular) that f i e l d was marked on the map as a black dot i n i t s position obtained from the co-ordinates given by the micrometer scale on the moving stage of the microscope* Traverses were taken across the section at intervals that varied depending on the size of the section. Every consecutive f i e l d on each traverse was examined. In most cases the fact that the degenerated terminal was larger than 2.5 u could be judged by eye; i n case of doubt i t was measured by means of a micrometer eye-piece. Typical units of degeneration are shown i n figures 52-55 and 64-65• We examined a total of approximately 6,00Q fields i n the dorso-medial nucleus i n our three control brains without finding 2 units of degeneration i n a single f i e l d . Maps of the control brains would therefore merely be blank. ( i i ) In the pontine nuclei these same c r i t e r i a proved to be quite unsuitable as this region normally contains a large number of bouton x Dark purple using this stains this criterion excludes particles of metallic precipitate which are jet black and colloid globules which are l i g h t purple and have moreover a less clearcut outline than have terminals. tera&neaux per f i e l d with a f a i r number f u l f i l l i n g the c r i t e r i a given above* Figure 50 shows a section from a normal pons mapped according to these c r i t e r i a . After examining sections from L-4, which alone of our brains appeared to show some degeneration i n the pontine nuclei, the following c r i t e r i a were chosen. On the map a f i e l d was shown as containing degeneration i f there were more than 50 boutons termineaux and 'degenerating terminals' of a l l kinds i n the f i e l d together with an obvious thinning of the normal plexus of fine unmyelinated fibres (figs. 70-71). Although fi e l d s with more than 25 boutons per f i e l d are frequent i n the normal pons as figure 50 shows we did not see any fiel d s i n the normal with as many as 50 boutons per f i e l d . But as we do not yet know the extent of individual variation i n this respect we introduced the second criterion - the thinning of the fibre plexus -although this re-introduces a subjective element into the c r i t e r i a . We were unable however to construct a workable objective criterion for the 'thinning' of a fibre plexus. ( i i i ) In the medial nmamillary nucleus the c r i t e r i a were fixed at two units of degeneration per f i e l d as i n (i) together with an obvious thinning and fragmentation of the normal plexus of fine unmyelinated fibres as i n ( i i ) ( f i g . 74-) • I t was noticable that the products of degeneration i n this region were not as large, nor did they stain so darkly as those seen i n (i) and ( i i ) . (iv) We were unable to reach satisfactory objective c r i t e r i a for degenerating fi b r e s . The mere size of the swellings along the course of the fibre would presumably depend to some extent on the i n i t i a l size of the f i b r e . Fragmentation, vacuolisation and heightened argyrophilia 18 do not lend themselves readily to recordable quantitative treatment which would not at the same time be unworkably clumsy. In our figures the presence of degenerating fibres was shown where there was more than one fibre in the field which appeared to be grossly degenerated (showing increased argyrophilia, gross fusiform or more irregular swellings in their course, vacuolisation and fragmentation)• (2) A method of presenting the information was developed so as to show, as nearly as possible, the actual position of each area of degeneration in the part concerned. This was done by preparing accurate maps of the part by means of readings taken on the micrometer stage of the microscope transferred to graph paper and the exact position of each field showing degeneration could then be inserted on the map after taking similar readings. 19 CHAPTER i n RESULTS L - l . As we mentioned above no degeneration was found anywhere i n this brain, except immediately around the wound where the appearance was the same as has been described previously i n the literature. Meyer ('4.9) found no evidence of degeneration i n a human case with a survival period of six days. L-2 and L-3. In each side of both these brains the extent of the degeneration was very similars (i) Thalamus. On each side of L-2 twelve coronal sections at approximately equal spacing through the dorso-medial nucleus were examined and maps were prepared from nineof these on each side, s i x of which are shown i n figures 14-19 (R) and four i n figures 20-23 (L). On the right side of L-3 twelve such sections were examined and maps prepared from eight of these, seven of which are shown i n figures 24-30. On the l e f t side of L-3 and L-4 (extreme posterior part) two such sections were examined and were found to be essentially similar to those taken from the same position on the right side of these brains. In L-2 (R and L) and L-3 R two additonal sections anterior to the rostral l i m i t of the dorso-medial nucleus and one section posterior to i t s caudal l i m i t were examined. Each of these sections included the f u l l extent of the thalamus, a l l nuclei of which were included i n the regular scanning. Maps were only prepared of regions showing degeneration. Figures 14-30 show representative examples of these maps and these show that there was degeneration i n the middle st r i p of the dorso-medial nucleus along almost i t s whole length ( f i g . 64)* This degeneration was more marked in the dorsal part of this s t r i p than i n the ventral part particularly r o s t r a l l y . I t extended a l i t t l e farther forward i n L-2 (R) than i n the others. I t was mostly i n the small-celled part but was not confined to i t . In any case the boundary between the two portions of the nucleus i s not always clear cut and so we have described the region of degeneration relative to the extent of the whole nucleus. The most medial and the most later a l portions of the nucleus have escaped the degeneration. No degeneration was seen i n the nucleus submedius. The apparent 'degeneration1 marked i n the nucleus parafascicularis i s not true degeneration as a comparison with the normal nucleus shows (figs. 51 and 66-67). This merely demonstrates, as has been previously reported (Smythies, Gibson and Purkis '55). that the nucleus parafascicularis i s unique amongst the thalamic nuclei i n having a relatively large number of large dark boutons termineaux and i s thus not a suitable location i n which to apply c r i t e r i a of degeneration appropriate to the other thalamic nuclei. ( i i ) Pre f r on to-pontine tract:. In L-2 a few fibres were seen degenerating i n the course of the fronto-pontine t r a c t (as; described by Beck '50). In L-3 many such fibres were seen degenerating immediately below the inferior l i m i t of the lesion ( f i g s . 35 and 68). The number of degenerating fibres seen rapidly decreased the further caudal to the lesion the section was taken (f i g s . 35-4-0). No definite signs of degeneration were seen i n the pons (compare f i g . 41 with f i g . 50). ( i i i ) Elsewhere. No degeneration was seen i n six sections through the hypothalamus i n each brain nor was there any to be seen i n numerous sections through the other nuclei l i s t e d above i n either brain. L-4. (i) Thalamus. Twelve sections spaced through the dorso-medial nucleus were examined and maps were prepared from seven of these, four of which are shown i n figures 31-34-• The type of degeneration i s shown i n figure 65. It w i l l be seen that the extent and type of degeneration i s essentially similar to that seen i n the other two brains. One point of interest i s the heavy degeneration seen i n the extreme posterior end of the nucleus i n the region of the pulvinar. As no such heavy degeneration was seen i n this region i n brains L-2 and L-3 this provides some evidence that the medial aspect of the frontal eulaminate cortex (undercut only i n L-4) projects particularly to the posterior end of the dorso-medial nucleus. On the other hand the place of origin of these fibres might be i n the most posterior part of the eulaminate cortex i n the dorsal convexity, also affected only i n L-4.. No degeneration was seen elsewhere i n the thalamus. ( i i ) Prefronto-pontine tract. Figures 42-4.6 and 69-71 show that the extent and nature of degeneration of the prefronto-pontine tract and i n the pons i s not significantly different from that reported by other workers. One possibly significant point i s the heavier degeneration i n the upper l/3 of the pons than i n the rest of the pons. I t should be noted that the sections made by the pathologist i n this brain were not true coronal sections but were very oblique being p a r a l l e l to that part of the fornix that runs through the hypothalamus. ( i i i ) Hypothalamus and elsewhere. Four sections through the mamillary body were examined three of which are shown i n figures 47-49. The type and extent of the degeneration (figs.~ 72-74) was essentially similar to that reported by Meyer ('49) except that there was a less cleareut antero-posterior difference* A small bundle of degenerating fibres was found running down beside the fornix i n the inferior thalamic radiation ( f i g * 47) possibly on i t s way to the mamillary body. No degeneration was seen i n four other sections examined through the . hypothalamus and septal nuclei* There was no degeneration seen i n the caudate nucleus, putamen, globus pallidus, substantia nigra, subthalamus, zona incerta or Forel's fi e l d s nor i n four sections taken at equal intervals along the whole length of the hippocampus* In the red nucleus there were more (normal looking) boutons than we had seen i n our normal controls but i n the absence of any other signs of degeneration a mere increase i n the number of boutons can not be regarded as evidence of degeneration u n t i l much more i s known about the extent of normal variation between different parts of the same nucleus i n one brain and the same parts of the same nucleus i n different brains* Cortex j An examination was also made of the extent of degeneration i n the cortex* In L - l and L-2, 68 sections (in each) from a l l parts of the cortex and i n L-2 40 sections from the frontal cortex were examined* No signs of degeneration were found except immediately around the wound (figs* 62-63)* I t was noticed that the same general features of bouton distribution and morphology that we have reported previously were present i n these brains* In L-4 20 sections of the frontal lobe and 7 sections of the occ i p i t a l and adjoining portions of the parietal and temporal lobes were examined* In the former degenerating terminals were seen as has been described by previous authors, progressively decreasing i n number from layer 6 outwards, the latter no degeneration was seen. CHAPTER TV' DISCUSSION These results confirm previous reports that the eulaminate cortex of the prefrontal region projects to the dorso-medial nucleus of the thalamus* The extent of this degeneration i s shown i n our figures* The minor variations i n the distribution of degeneration i n these three brains may prove to have significance i f compared with the results of many more such investigations. The most marked of the variations l i e s i n the heavy degeneration i n the extreme posterior part of the nucleus i n the only case where the lesion undercut the cortex on the medial aspect of the hemisphere and extended to the most posterior part of the eulaminate cortex on the dorsal convexity. We were unable to confirm previous reports (Meyer'49, Martinez '55) that the nucleus submedius i s also involved* The morphology of the boutons i f l the normal nucleus parafascicularis ( f i g s . 65-66) should be taken into account i n evaluating the presence of degeneration i n this.nucleus and i n the rather ill - d e f i n e d region between i t and the nucleus submedius* Our results also confirm Meyer's observation ('4-9) that a lesion encroaching upon the granular cortex on the dorsal convexity of the frontal lobe projects to the medial mamillary body, particularly i t s ventral part. Our results also confirm that there are no significant hypothalamic connexions from purely eulaminate regions of the frontal lobe outside the o r b i t a l regions (which were not affected i n any of our specimens)• The prefronto-pontine tract i s also involved i n a l l oxer brains showing degeneration. The heavier involvement i n L-4 may 25 merely be an indication of the noci-fugal spread of degeneration i n fibre tracts shown clearly i n this tract i n L-3 and described i n the rabbit by Glees, Meyer and Meyer (*4-7). We have also attempted to set up objective quantitative c r i t e r i a of degeneration and have u t i l i s e d a mapping method of plotting the location of degeneration. However, these c r i t e r i a are not yet completely objective as we could not find satisfactory quantitative c r i t e r i a for fibre degeneration nor for the disintegration of a fine unmyelinated fibre plexus. The l o c a l differences i n the picture of degeneration seen are also interesting. In the dorso-medial nucleus of the thalamus the tendency was to produce large (often 3-5 u) solid, or nearly solid, masses without much sign of any fragmentation of the fine unmyelinated plexus (figs. 52-55). I t was also noteworthy that the picture seen at 12 days hardly differed from that seen at 7 days. In the medial mamillary body the picture of degeneration was a marked disintegration of the fine unmyelinated fibre plexus into a large number of argentophil masses, mainly solid, but on the average considerably smaller (and less argyrophilic) than those seen i n the dorso-medial nucleus and often not much more than beads ( f i g . 1U) • In the pons there was an increase i n the number of boutons seen (with a high proportion of larger terminals) together with a fragmentation and disappearance of the fine unmyelinated fibre plexus (figs. 70-71). This account only describes what may be seen at certain periods after the injury. Examinations at other post-operative periods might be expected to give different microscopic pictures. / 26 F i n a l l y , f rom our s t u d y o f the normal d i s t r i b u t i o n and morphology o f boutons termineaux we can t e n t a t i v e l y suggest t h a t o u r •dorso- m e dia l* c r i t e r i a a r e s u i t a b l e f o r a l l p a r t s o f the f o r e b r a i n except the nucleus p a r a f a s c i c u l a r i s o f the thalamus, the mesocortex, s u b s t a n t i a n i g r a and globus p a l l i d u s , and p a r t s o f the amygdaloid complex* A r e a U o f the n e o c o r t e x and the s u b i c u l u m might g i v e r i s e t o some d i f f i c u l t i e s o f i n t e r p r e t a t i o n * I n the m e d i a l m a m i l l a r y body the s i z e and depth o f s t a i n i n g o f the products o f d e g e n e r a t i o n were n o t so marked as t o r e n d e r the c r i t e r i a o f d e g e n e r a t i o n based s o l e l y on t h i s f e a t u r e as c e r t a i n as one would w i s h thus n e c e s s i t a t i n g the i n c l u s i o n o f f r a g m e n t a t i o n o f the f i n e f i b r e p l e x u s . T h i s disadvantage might a l s o be encountered i n o t h e r n u c l e i i n which we d i d n o t have the o p p o r t u n i t y o f examining d e g e n e r a t i o n . S p e c i f i c c r i t e r i a can o n l y be s e t up f o r each nuc leus and c o r t i c a l a r e a a f t e r a thorough s t u d y o f the form o f d e g e n e r a t i o n i n each p a r t - a n d o f the form o f the normal s y n a p t i c morphology i n each p a r t . 27 CHAPTER V SUMMARY A study has been made of the extent of terminal degeneration i n four lobotomised brains using a si l v e r method. We have confirmed previous reports that the eulaminate cortex of the frontal lobe outside the orbital region projects exclusively to (i) the dorso-medial nucleus of the thalamus and vre have localised this projection to a st r i p along the median part of the nucleus i n the greater part of i t s length, and ( i i ) to the pontine nuclei. In one brain the lesion encroached upon agranular cortex and here degeneration was also found i n the medial mamillary body but not elsewhere. Differences i n the microscopic appearance of terminal degeneration i n the various regions has also been described. We have also paid particular attention to the method of terminal degeneration i t s e l f and have endeavoured to place this on a more objective basis, using quantitative c r i t e r i a of  degeneration wherever possible. BIBLIOGRAPHY 28 ADEY, W. R. " 1951 An experimental study of the hippocampal connexions of the cingulate cortex i n the rabbit. Brain, 24•* 233-247. BARNARD, R. I. 1940 Experimental changes i n end-feet of Held-Auerbach i n the spinal cord of the cat. J . Comp. Neur., 23.: 235-266. BECK, E. 1950 The origin, course and termination of the prefronto-pontine tract i n the human brain. Brain, 22: 368-391. BECK, E., A. METER AND J. LE BEAU 1951 Efferent connexions of the human prefrontal region, with reference to fronto-hypothalamic pathways. J . Neurol. Neurosurg. Psychiat., 14: 295-302. BLACKS TAD, T., A. BRODAL AND F. WALBERG 1951 Some observations on normal and degenerating terminal boutons i n the inferior olive of the cat. Acta Anat., 11: 461-477. BRODAL, A. 1949 Spinal afferents to the l a t e r a l reticular nucleus of the medulla oblongata i n the cat. An experimental study. J . Comp. Neur., °1: 259-295. BRODAL, A., T. BLACKSTAD AND F. WALBERG 1950 Termination of spinal afferents to inferior olive i n cat. J . Neurophysiol., 13: 431-454. CAJAL, S. RAMON Y 1911 Los fenomenos precoces de l a degeneracion traumatica de los cilindros-ejes del cerebro. Trab. del Lab. di invest, b i o l . Madrid, 2s 39-95. ^ Papers not actually consulted are marked with a star. 29 CLARK, W. E. LE GROS, AND M. MEYER 194-7 The terminal connexions of the olfactory tract i n the rabbit. Brain, 70: 304.-328. DE CASTRO, F. 1930 Recherches sur l a degeneration et l a regeneration du systeme nerveux sympathetique• Quelques observations sur l a constitution des synapses dans les ganglions. Trab. del Lab. d i invest, b i o l . Madrid, 26 : 357-4-56. FEDOROW, B. G., AND S. J. MATWEJEWA 1935 La structure des connexions interneuronales dans le systeme nerveux autonome de l a grenouille. Trav. Lab. Resherches B i o l . Univ. Madrid, _{0: 378-4-01. GETZ, B. 1952 The termination of spinothalamic fibres i n the cat as studied by the method of terminal degeneration. Acta Anat., 16: 271-290. GIBSON, W. C. 1937 Degeneration of the boutons terminaux i n the spinal cord. An experimental study. Arch. Neurol, and Psychiat., 28: 1L45-1157. 194-0 Degeneration and regeneration of sympathetic synapses. J . Neurophysiol., 2i 237-247. GLEES, P. 1941 The termination of optic fibres i n the l a t e r a l geniculate body of the cat. J . Anat., 7j_: 4-34-44-0. 1942 The termination of optic fibres i n the l a t e r a l geniculate body of the rabbit. J . Anat., 76: 313-318. .1944 The anatomical basis of cortico-striate connections. J . Anat., 7J_: 47-51. GLEES, P. AND W. E. LE GROS CLARK 1941 The termination of optic fibres i n the l a t e r a l geniculate body of the monkey. J . Anat., 75: 295-308. 30 GLEES, P., A. MEIER AND M. MEYER 194-6 Terminal degeneration i n the frontal cortex of the rabbit following the interruption of afferent fibres. J . Anat., 80: 101-106. HOFF, E. C. 1932 a Central nerve terminals i n the mammalian spinal cord and their examination by experimental degeneration. Proc. Roy. Soc. Lond. B., J^i 175-188. 1932 b The distribution of the spinal terminals (boutons) of the pyramidal tract, determined by experimental degeneration. Proc. Roy. Soc. Lond. B., 226-237. i 1935 Corticospinal fibres arising i n the premotor area of the monkey. Distribution of bouton terminations. Arch. Neurol. and Psychia't., 22.'- 689*697. LAWEENTJEW, B. J . 1934- Experimentell-morphologische Studien tlber den feineren Bau des autonomen Nervensystems weitere Unter suchungen fiber die Degeneration und Regeneration der Synapsen. Zrschr. f . mikr. anat. Forsch., 25_: 71-118. LEVI, G. 1932 Uber das mutmassliche Bestehen von sympathischen Zellen i n den kranialen und spinalen ganglien. Bernerkungen zu einer Arbeit von F. Kiss, Anat. Anz., 22: 187-190. MARTINEZ, A. 1955 Some efferent connexions of the human frontal lobe. J . Neurosurg., 12,: 18-25. MEYER, M. 194.9 Study of efferent connexions of the frontal lobe i n the human brain after leucotomy. Brain, 22: 265-296. MINCKLER, J. 194.0 The morphology of the nerve terminals of the human spinal cord as seen i n block silver preparations, with estimates of the to t a l number per c e l l . Anat. Rec, 22* 9-25. 31 NIKOLA JEW, W. 1893 Zur Frage die innervation des Froschherzens. Arch. f . Physiol. Suppl., 67-73. PHALEN, G. S., AND H. %.. DAVENPORT 1937 Pericellular end-bulbs i n the central nervous system of vertebrates. J . Comp. Neur., 68: 67-81. RANSON, S. W., AND P. R. BILLINGSLEY 1918 The superior cervical ganglion and the cervical portion of the sympathetic tract. J. Comp. Neur., .22: 313-358. SCHIMERT, J. 1938 Die Endigungsweise des Tractus vestlbulospinalis. Ztschr. f . Anat. u. Entwicklungsgesch., 108: 761-767. SERENI, E., AND J. Z. YOUNG 1932 Nervous degeneration and regeneration in cephalopods. Pubbl. d. stazione Zool. d i Napoli, 12* 173-208. SMYTH EES, J . R., W. C. GIBSON AND V. A. PUREES 1955 The distribution and morphology of boutons termineaux i n the human cerebrum. J . Comp. Neur!., i n press. TUCKETT, I . L. 1896 On the structure and degeneration of non-myelinated nerve fibres. J . Physiol., 12* 267-311. WALL, P. D., P. GLEES AND J. F. FULTON 1951 Corticofugal connexions of posterior orbital surface i n Rhesus monkey. Brain", 24 s 66-71. i F i g . 1 F i g . 2 F i g . k l _ . F i g . 5 Fig. 6 Fig. 7 I I 1 e i F i g . 8 ! I F i g . 9 e Fig. 10 F i g . ir r ! Fig. 12 j 1 ! F ie° ^ ; : Fig. 15 ] 1 Fig. 17 Fig. 18 Fig. 20 i I i F i g . 21 F i g . 22 ! F i g . 23 I ) I Fig i r i I F i g . 26 1 F i g . 27 A.M. M.T. Pa Cv M I I F i g . 33 ) F i g . 34. : F i g . 35 F i g . 36 F i g . 39 F i g . A3 F i g . U I F i g . Ul i Fig. 48' Fig. 49 i 1 F i g . 51 t I F I G . 4A. F I G . 4B. F I G . 4 A .—A n outline of the right half of the spinal cord at the seventh post-thoracic segment, from a cat completely de-afferented on the right side of the lumbar enlarge-ment. The drawing was made from six sections, and each dot represents a cell upon which degenerating boutons were found. Cat 2, operation 2. (Camera lucida drawing.) F I G . 4 B . — A diagram showing the manner of termination of afferent nerves in the grey matter of the cord suggested by the location of degenerated boutons in the grey matter of de-afferented cords. The way i n which cells in the mid-region connect with ventral horn cells is not suggested, as implied by the broken line. ram. Fig. 4 (experiment 2).—Sections of the spinal cord at the seventh cervical and sixth postthoracic segments, showing the distribution of bouton degeneration in the spinal gray matter of a macaque killed four days after ablation of the right premotor area. The black circles and triangles have the same significance as in figure 2. (The diagram was drawn with a projector.) rn.c. ventral ii't forelimb titr hindlimb F i g . 7 To tin- left :i composite d iagram of the findings in this study. The termina l iiroii of fillers f rom tlic cervical segments is indicated by r ings, the area for fibers f rom below mid-thoracic by dots ( fo r tlie sake of s impl ic i ty termed fore l iml i and h ind l imb areas) . To tlie r ight ;i series of transverse sections through the latci ' i i l ret icnl i i r nucleus showing the d is t r ibut ion of retrograde cell changes fo l low ing :i pa iavc rmian incis ion of tlie cerebellum ("43) . Black denotes areas max ima l ly changed, cross hatchings intermediate, and simple hatchings s l ight ly changed areas. The figures of the sections to the right refer to their order in the complete d iagram in the previous paper, and the heavy hor izontal l ines indicate the level of each section with reference to tlie longi tudinal sections to the left. Abbrev ia t ions , as in figure dorsal Via. A. Diagram of findings in cat .Sp. C . L . 12. Lesion of cord at C_. ;. Above, series of horizontal sections through inferior olive. Its different parts are indicated (abbreviations as in Kig. 1). Dotted areas show parts in which terminal degeneration of fibers and boutons is present, density of dots giving an approximate impression of intensity of degeneration. Wavy vertical lines indicate coarse ascending degenerated fibers. Below, two sections through spinal cord; left, drawing of superimposed cell-stained sections from Cj_ ; i, showing total extent of lesion (hatchings); right, diagram of ascending degenerated fibers seen in Marchi sections from C,. L: left. H: right. N .r . l .: Lateral reticular nucleus. F i g . 59 Fig. 2. Diagram of the findings in oat Sp. C. L . 21. Lesion nf the cord at C|. Ab-ove, series of frontal sections through the thalamus. The main nuclei are indicated as in figure 1. The dotted areas show where terminal de-generation is present, and the density of the dots give an approx-imate impression of the intensity of the degeneration. Below, a section through the spinal cord at Cv • showing the lesion. The area totally damaged is indicated black, areas partly damaged are hatched. Sp.CL21 C i ' ) Fig. 60 | r i I FIG. 16 {Case 4). i i i F i g . 61 '• F i g . 62 Fig. 63 F i g . 64. I F i g . 65 Fig. 66 Fig. 67 Fig. 68 F i g . 69 Fig. 71 

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