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Variations in the fine structure of layers III to VI of the somatic sensory cortex have been described. Layers III and IV may be readily distinguished from one another and from layers V and VI, but within the latter two layers there is such a slow gradient of change that no clear-cut line of junction can be drawn between them. Layer III is characterized by the presence of many large apical dendrites ascending vertically through it from pyramidal cells in all layers to reach layer I. In parallel with these are many small unmyelinated axons which contain flattened synaptic vesicles and terminate on transversely orientated dendrites in symmetrical synaptic complexes. The remainder of the neuropil is filled by large numbers of dendritic spines receiving axon terminals which contain spherical vesicles and which terminate asymmetrically. In layer IV there is a marked increase in the number of small myelinated axons ascending from below and ramifying within it. Embedded in the neuropil among these are many small non-pyramidal neurons whose somata and small, irregular dendrites are covered in axon terminals. Also present, and particularly concentrated at the junction with layer III, is a meshwork of fine unmyelinated axons which contain flattened vesicles and terminate in an en passant manner as symmetrical type synapses. Most of these axons are orientated transversely. A larger axon terminal which ends in asymmetrical complexes on small dendritic shafts and spines and which may be the terminal of thalamo-cortical axons is only found in any quantity in this layer. On descending into layers V and VI there is a progressive increase in the number of large myelinated fibres and glial cells, and a progressive diminution of neuronal elements, particularly dendritic spines. Some large non-pyramidal cells resembling the smaller ones on layer IV are present in layer VI.

Layers I and II of the somatic sensory cortex are clearly distinguishable with the electron microscope because of characteristic differences in the number, type and orientation of neurons and dendritic and axonal ramifications. Layer I may be subdivided into: (i) a subpial astrocytic layer immediately deep to the basement membrane of the cerebral surface; (ii) a superficial quarter consisting of bundles of small myelinated axons and large numbers of small axon terminals which contain spherical vesicles and end in asymmetrical synaptic complexes mainly on large dendritic spines. Most of these terminals are derived from a dense feltwork of fine unmyelinated axons which are especially concentrated at the junction of the superficial and deep parts of layer I; (iii) a deeper three quarters with similar features to the above but with the additional characteristic of many obliquely orientated large dendrites which are the diverging branches of apical dendrites ascending from deeper layers. Small pyramidal neurons dominate layer II, but among them are a small number of non-pyramidal neurons whose beaded dendrites are covered with axon terminals. Large apical dendrites traverse this layer, and in addition to the typical asymmetrical synapse on dendritic spines, a few symmetrical types appear. These are derived from thin unmyelinated axons orientated horizontally within the layer, and the terminals contain many small flattened or pleomorphic synaptic vesicles.

The nature and immediate postoperative course of experimental degeneration of axon terminals have been studied in the somatic sensory cortex. The first somatic sensory area was examined at intervals of 2 to 6 days following lesions in the thalamus, opposite cortex or ipsilateral second somatic sensory area. There is a characteristic sequence of degenerative changes which affects the terminals of each of the afferent fibre systems studied. This commences as a simple, though marked, increase in electron density of the axoplasm with no loss of synaptic vesicles and little alteration in the size or shape of the terminal. Following this, there is a progressive loss of vesicles and disruption of the mitochondria with shrinkage of the terminal and its compression, invasion and fragmentation by astroglial processes. There is evidence that many fragments are phagocytosed by the invading astroglia but a thin sliver always remains attached at the synaptic contact zone. Within the range of survival periods used, no changes affect the synaptic region nor the postsynaptic profile and if the latter is a dendritic spine, it is not detached from the parent dendrite. Changes in degenerating axons are similar, except that the largest thalamo-cortical fibres show a stage of neurofilamentous hyperplasia. In the cortex at a distance from the lesion only smaller astrocytic processes are involved in breaking down the degenerating products; close to a lesion, however, all astrocytic processes and perikarya become involved and many atypical glial cells which are difficult to classify as astrocytes or oligodendrocytes become visible; the vascular pericytes also display large heterogeneous dense bodies and other inclusions.

The ascending thalamic connexions of the general sensory cortex of Macaca have been studied by recording the retrograde cell degeneration in the posterior ventral nucleus of the thalamus following selective lesions involving the cytoarchitectonic areas o f the postcentral gyrus. Area 3 (of Brodmann) receives connexions from the entire rostro-caudal extent of the nucleus; they are derived from most of the cells in the rostral half and from at least 50% of the cells in the caudal half. Area 1 receives the exclusive projection of a proportion of the cells (up to 30% in the caudal half of the nucleus), and probably also collaterals from other axons which terminate mainly in area 3. The retrograde degeneration following lesions of area 2 provides no evidence that this area receives the exclusive projection of any of the cells of the posterior ventral nucleus, but there is evidence that it receives collaterals of axons terminating mainly in areas 3 and 1. Destruction of any one of the cytoarchitectonic areas of the postcentral gyrus results in a partial diffuse degeneration over the whole cross-sectional area of the ventro-lateral nucleus at different levels. Only when a complete sector of the postcentral gyrus is destroyed, involving all three cytoarchitectonic areas, is there a sharply circumscribed lamina of retrograde degeneration extending throughout the rostro-caudal extent of the nucleus. The nucleus lateralis posterior of the thalamus projects to the parietal cortex; there is no evidence that it has any connexion with the general sensory cortex. The results of these experiments are discussed in relation to clinical observations of dissociated sensory loss following lesions of the postcentral gyrus in man.

The thalamic projection to the visual cortex has been studied in the cat and monkey by experimental light and electron microscopic techniques. After large lesions of the lateral geniculate nucleus degeneration is confined to the ipsilateral hemisphere. In the cat it is found in areas 17, 18 and 19 and in the lateral suprasylvian area, terminal degeneration occurring predominantly in layer IV, with less in layers I, III and V ; fibre degeneration crossing layers VI and V towards layer IV is coarser in area 18 than elsewhere. Some fine horizontal degenerating fibres are seen in layer I. In the monkey terminal degeneration is restricted to area 17; again degenerating fibres ascend to layer IV where there is dense fragmentation, but in contrast to the cat there is also a second, less dense, but distinct, band in layer Illb. A little fine, horizontal fibre degeneration is present in layer I and there is slight terminal degeneration in this site and in layer V. Electron microscopy shows that degenerating terminals are recognizable in the visual cortex at several stages according to survival period, but that most stages can exist simultaneously in any one site, and that all are associated with asymmetrical membrane thickenings. Mapping of electron microscopic sections confirms the laminar pattern seen with the light microscope. In area 17 of the cat and monkey and in area 19 of the cat over 80% of degenerating terminals end on dendritic spines, the rest making synaptic contact mainly with dendritic shafts, and very few with the soma of stellate cells, but in area 18 some 10 % are related to stellate cell bodies. In layer IV of all areas degenerating terminals tend to occur in clusters which are separated by approximately 100μm. Where degenerating thalamic afferents end on cell somata or varicose dendrites almost all are identifiable as derived from stellate cells. Although it is difficult to identify positively the parent dendrites bearing the spines which receive the majority of the thalamo-cortical afferents, it is suggested that some, at least, of them may also originate from stellate cells.

Two main types of neuron may be distinguished electron microscopically in the somatic sensory cortex. Pyramidal neurons have a characteristically triangular perikaryon with a high content of ribonucleoprotein consisting mainly of free ribosomes; the nucleus usually shows a single small indentation. Nonpyramidal neurons, which may be large or small, have a higher concentration of all intracytoplasmic organelles and particularly of long cisternae of rough-surfaced endoplasmic reticulum forming Nissl bodies. The nucleus is often deeply indented and crenellated. The two cell types differ also in the nature of their dendritic ramifications and particularly in their synaptic relationships. The majority of axon terminals ending on pyramidal neurons contact dendritic spines and relatively few end on the shafts of dendrites or on the perikaryon. Synapses on spines are typically of the type in which the synaptic thickenings are asymmetrical and the synaptic vesicles spherical. Such synapses, even when they occur on the shafts of pyramidal cell dendrites, are usually associated with a ‘spine apparatus’. Most of the few synapses on the dendritic shafts and somata of pyramidal cells are associated with symmetrical membrane contacts and small, flattened or pleomorphic vesicles. Terminals of this type are commonly en passant endings of long, thin unmyelinated axons oriented vertically or transversely within the cortex. The somata and the usually irregular dendrites of non-pyramidal neurons are typically covered in axon terminals most of which contain flattened vesicles and end in symmetrical complexes, but a few may contain spherical vesicles and end asymmetrically. The axon hillocks and initial segments of both types of cell are postsynaptic to axon terminals containing small, flattened vesicles and ending symmetrically.

From time to time cases of diarrhóa arise in asylum practice which are not due to any specific cause.∗

The termination of fibres from the cerebral cortex and thalamus upon the dendritic spines of the medium spiny cell of the caudate nucleus has been studied with the Golgi method. Lesions were placed in the cerebral cortex, thalamus or cerebral cortex and thalamus of adult cats and kittens. After survival periods of between 6 and 52 weeks the animals were perfused with a mixture of formaldehyde and glutaraldehyde and the caudate nuclei impregnated by a Golgi technique. The distribution of spines along the dendrites of the medium spiny cell was determined in normal material by counting them over 20 $\mu m$ lengths of the dendrites, and was compared with their number and distribution after the various lesions. The density of spines on the dendrites varies with the distance from the cell body. The first 20 $\mu m$ length of dendrite is spine free, but thereafter the number increases to a peak between 60 and 80 $\mu m$ from the cell body after which the number per 20 $\mu m$ length decreases. The distribution pattern does not alter after any of the lesions, although the overall number of spines decreases. The decrease after lesions in the cerebral cortex or thalamus is the same, and after a combined lesion of thalamus and cortex is twice as great indicating that the fibres from both these regions end upon spines of the same cells. Statistical analysis shows that these results are significant.

The synaptic organization of the caudate nucleus appears to be homogeneous with no specialized groupings of axon terminals and postsynaptic profiles. The nerve terminals in the caudate nucleus fall into two size groups, one about 1 fim in diameter and the other about 5 /itn diameter. The smaller size group, which comprises the majority of terminals, may be subdivided into three varieties on the basis of vesicle morphology and the type of membrane thickening. Most contain round, 45 nm diameter vesicles and are associated with asymmetrical membrane thickenings. Others contain 48 nm diameter, polymorphic vesicles, which become flat in material washed in cacodylate buffer, and are associated with symmetrical membrane thickenings. A few other terminals with symmetrical membrane thickenings contain flat 42 nm vesicles. The large terminals contain round 45 nm diameter vesicles and have asymmetrical membrane thickenings. Axon terminals with asymmetrical membrane thickenings are found most frequently in contact with dendritic spines, but also with dendritic shafts and cell somata. Terminals with symmetrical membrane thickenings contact dendritic shafts and cell somata, and occasionally dendritic spines with which a terminal with asymmetrical thickenings is also making contact. The two types of terminal with symmetrical contact regions also form synapses onto the initial segments of axons. It is probable that such contact regions are invariably associated with cisternal organs in the initial segments. Serial synapses are found occasionally.

At the last February meeting of the Manchester Pathological Society we made a preliminary communication upon this subject, limited to a description of the changes found in the cortical nerve-cells and the descending degenerations in the spinal cord. Since then we have examined a much larger number of cases, and can therefore give a fuller description, with observations upon other points in the morbid anatomy of general paralysis of the insane.

An electron microscopic study has been made of the axon terminal degeneration in the caudate nucleus in the cat after lesions in either the cerebral cortex, the thalamus, the cerebral cortex and the thalamus, the midbrain or within the caudate nucleus. Degenerating axon terminals can be recognized after a survival period of 4 days as dark, shrunken profiles with indistinct vesicles. After shorter survival periods the degenerating terminals contain swollen vesicles and have pale cytoplasm. After lesions in all the above sites there is degeneration of fine myelinated and nonmyelinated fibres. The degenerating terminals of all the afferent fibres to the caudate nucleus have asymmetrical membrane thickenings and end mainly on dendritic spines with a small proportion in contact with peripheral dendrites; after damage of the cerebral cortex or thalamus a few of the degenerating terminals also end upon main stem dendrites and cell bodies. The projection from the ipsilateral cerebral cortex is greater than that from the thalamus, which in turn is heavier than that from the contralateral cortex or midbrain. After lesions within the caudate nucleus degenerating terminals with symmetrical membrane thickenings are found in a region extending approximately 450 pm from the damaged part of the nucleus. These terminals make contact with nerve cell somata, main stem and peripheral dendrites and the initial segments of axons. After such a lesion of the caudate nucleus degenerating axon terminals with symmetrical membrane thickenings are also seen in the globus pallidus and the substantia nigra.

In a series of experiments, the extrinsic afferent pathways to the somatic sensory areas have been selectively interrupted and the distribution and mode of termination of degenerating synaptic endings studied at intervals of 2 to 6 days. Degenerating commissural fibres terminate on spines attached to dendrites of medium and small size in all cortical layers, but the endings are concentrated in the deeper parts of layers I and III and in layer IV. Cortical association fibres passing from SII to SI end on spines of small and medium-sized dendrites mainly in the intermediate layers (III, IV and V) of the cortex, but a small number are invariably seen in the molecular layer. Some of the latter are probably derived from thin myelinated axons which spread radially from a lesion and run just beneath the pia mater. Degenerating thalamo-cortical axons terminate on spines and to a lesser extent on shafts of dendrites of small diameter, mainly in layer IV but with overlap into adjacent parts of layers III and V and with an additional small but consistent number ending in the molecular layer. Thus, the molecular layer and layer IV receive the terminations of all extrinsic afferents, while the relations of these to the other laminae and their mode of termination is, in each case, slightly different. One interpretation of the results is that all three sets of extrinsic afferents terminate in the middle portion of the apical dendritic tree of pyramidal neurons, and that thalamo-cortical fibres have additional terminals on stellate neurons. The functional implications of this arrangement are discussed.

The normal fine structure of the ventroposterior, and medial and lateral geniculate nuclei of the thalamus has been examined in the cat, particular attention being paid to localized aggregations of pre- and postsynaptic profiles which have been termed 9glomeruli9, and which are common to these and certain other thalamic nuclei. The ventroposterior and medial geniculate nuclei show many similarities. Their glialensheathed glomeruli have one (or occasionally two) central dendrites which are usually bulbous side branches of main stem dendrites arising from neurons in the nuclei. These side branches commonly contain bundles, rings and whorls of neurofilaments. Two types of axon terminal complete the glomerulus: every glomerulus contains one (or at most two) large dark terminals; these have a heavy concentration of synaptic vesicles and a dense background cytoplasm and are derived from axons of medium diameter. They make asymmetrical synaptic contacts with the central dendrite and (axo-axonically) with the second type of terminal. This second type is a pale terminal with a clear cytoplasm and contains fewer synaptic vesicles than the large dark type; several pale terminals occur in a single glomerulus and they make short symmetrical synaptic contacts with the central dendrite only. Both types of axon terminal are also joined to the central dendrite by multiple adhesion plaques. The pale axon terminals are bulbous enlargements of long beaded processes; these come off very large unmyelinated profiles which resemble axon hillocks and may, therefore, be recurrent collaterals of thalamo-cortical relay cells or axons of interneurons. The commonest type of axon terminal outside the glomeruli is a small dark type which makes asymmetrical synaptic contacts with dendrites and the long beaded parent processes of the pale axon terminals, each of which may enter glomeruli close to or at some distance from this synapse. Dendrites beyond the point at which they enter glomeruli may be completely surrounded by small dark terminals. In the dorsal lateral geniculate nucleus, the same types of profile are present, but the organization of the glomerulus is slightly different in that the large dark terminal occupies the central position and several dendrites and many pale axon terminals are clustered peripherally. Small dark axon terminals, again, end outside the glomeruli, mainly on dendrites or pale processes which ultimately enter glomeruli. Axo-somatic synapses are present in all three nuclei but are singularly rare.

The retrograde cell degeneration in the lateral geniculate nucleus of the cat has been studied after lesions of the visual and adjoining areas of the cortex. Following lesions which are limited to area 17, the medium and small cells of the main laminae of the nucleus degenerate; damage restricted to area 18 does not result in any localized, severe degeneration, but com­bined destruction of areas 17 and 18 causes all the cells—large, medium and small—of the main laminae and the central interlaminar nucleus to degenerate. Cellular change in the medial interlaminar nucleus is only found after involvement of area 19. When the cortex of the middle suprasylvian gyrus is removed in addition to these areas the degeneration in the lateral geniculate nucleus is much more severe, and there is loss of the laminar pattern due to severe gliosis in the central interlaminar nucleus. There is a well-defined topical organiza­tion in the geniculo-cortical projection, and in the antero-posterior dimension it is the same to all areas of the visual cortex, anterior parts of the nucleus projecting anteriorly and posterior parts posteriorly. Medial parts of the main laminae are related to the lateral part of area 17 and to the medial part of area 18, and lateral parts of the laminae project to the medial part of area 17 and to the lateral part of area 18. After partial lesions which involve both areas 17 and 18 the cellular degeneration affects the laminae differentially along their antero-posterior extent, that in lamina A being the most anterior and that in lamina B the most posterior; in sagittal sections such a band, or column, of degeneration passes from antero-superior to postero-inferior at right angles to the plane of the laminae.

Several cases of insanity following injuries to the head have been admitted to the County Asylum, Prestwich, of late, Although we do not assert that there is a special form of insanity arising from “trauma,” yet there are certain types of mental derangement produced either directly or remotely by injuries. The five cases which are described below are of special interest and are good examples of certain of these types. None of them proved fatal, but the diagnosis is so clear in each of them that the pathological processes involved may be accurately described.

Beauty Seedless grape pigments were isolated and identified by chromatographic, spectral and chemical properties. The pigments were identified as delphinidin-3-glucoside, petunidin-3-glucoside, malvidin-3-glucoside, peonidin-3-glucoside, malvidin-3-glucoside acylated with caffeic acid and malvidin-3-glucoside acylated with p-coumaric acid. Beauty Seedless grapes contained 62 mg anthocyanins per 100g fresh grapes and malvidin derivatives accounted for 73% of the total anthocyanins.

The ion-exchange behaviors of succinic, malic and tartaric acids on Amberlite resins are evaluated. Retention and detector response data on silyl derivatives of several organic acids are presented. A procedure for the purification of grape juice by use of ion-exchange resins prior to gas chromatography is described. The malic and tartaric acid contents (g/100 ml juice) respectively, of commercially acceptable grapes were found to be: Thompson Seedless 0.25, 0.90; Cardinal 0.31, 0.91; Beauty Seedless 0.19, 0.62; Perlette 0.26, 0.97; Exotic 0.27, 0.36; and Robin 0.41, 0.37.

The existence of corticofugal fibres passing from the main sensory areas of the cerebral cortex to the thalamic relay nuclei has been confirmed by an electron microscopic study of the ventropo sterior, and medial and lateral geniculate nuclei 3 and 4 days after lesions in the appropriate cortical area. The degenerating cortico-thalamic fibres belong to the smallest group of myelinated axons found in the nuclei. Four days after a cortical lesion many degenerating axon terminals are found in all three nuclei, often in small clusters. These usually terminate outside the synapticglomeruli of then ucleus on stem dendrites and on the long parent profiles of the pale axon terminals of the glomeruli. In many cases, these dendrites and long parent processes enter a glomerulus close to or at some distance from the degenerating synapse. In a few cases, a degenerating terminal ends in closer relation to a glomerulus, usually on one of the more peripherally placed pale axon terminals. These findings indicate that the terminals of cortico-thalamic fibres belong to the small dark group of axon terminals described in the normal nuclei, but the persistence of many small dark terminals after total hemidecortication suggests that others have a subcortical origin. Four days after a cortical lesion, degeneration of the cortico-thalamic terminals is at a very advanced stage, whereas at a survival period of three days, only a few terminals show unequivocal degeneration. The degenerative change thus appears to be sudden and rapid.

The cellular changes in the mamillary nuclei following lesions of the cingulate cortex, the anterior thalamic radiation and the anterior thalamic nuclei have been studied in rabbits varying in age from 10 days to young adults. Distinct cellular degeneration ranging in severity from slight cell shrinkage to complete cell loss occurs in the medial and supra-mamillary nuclei subsequent to the retrograde changes in the anterior thalamic nuclei. The severity of this ‘retrograde transneuronal degeneration’ is a function of the age of the animal at the time of operation and of the post-operative survival period. With the aid of this technique, it has been shown that the caudal part of the pars anterior and the ventro-lateral two-thirds of the pars medialis of the medial mamillary nucleus project to the antero-medial nucleus of the thalamus, the pars basalis to the antero-dorsal nucleus and the pars posterior to the antero-ventral nucleus. No changes were observed in the lateral mamillary nucleus in any of the experiments.

A study has been made of the origin and course of the centrifugal fibres in the visual pathway of the pigeon using the Nauta method. Lesions in the mid-brain involving the isthmo-optic nucleus result in fibre degeneration which can be traced through the isthmo-optic tract to the chiasma and thence into the contralateral optic nerve and retina. In the retin a severe degeneration is found throughout the optic nerve layer, and occasional degenerating fibres can be traced through the ganglion cell layer to the inner aspect of the bipolar cell layer. Here they terminate in endings similar to those described by Cajal (1889) and Dogiel (1895) in relation to amacrine cells. The projection to the retina is completely crossed. Counts of the number of cells in the isthmo-optic nucleus indicate that the number of centrifugal fibres is approximately 10000; they form 1 % of the total number of fibres in the optic nerve. The isthmo-optic nucleus receives afferents from the tectum, and in this projection there would appear to be a well-defined organization.

Wiesel and Hubel 7 have described the occurrence of transneuronal degeneration in the lateral geniculate nucleus after visual deprivation caused by eyelid suture in kittens. Recently, evidence has accumulated that this degeneration may not be due simply to changes in afferent activity as previously thought, for after closure of one eye in kittens the transneuronal atrophy in the relevant laminae of the lateral geniculate

The caudate nucleus of the cat appears to be homogeneous when examined with the light or electron microscope, except for a layer beneath the ependyma where there is a high concentration of glial cells and few neurons. In sections of brains stained with thionin the nerve cells in the caudate nucleus fall into three size groups: less than 8 $\mu m$ , 9 to 18 $\mu m$ , greater than 20 $\mu m$ . Examination of material impregnated with the Golgi technique shows that there are six cell types (one small, four medium and one large), and these are distinguishable on the basis of the size of the cell somata and the appearance and arrangement of their dendrites. One type of medium cell with many dendritic spines forms over 95% of the cell population. The large and one medium cell type are tentatively identified as the source of the efferent fibres of the nucleus. These efferent fibres and the axons of the remaining medium cell types have collateral branches. Three groups of possible afferent fibres have been identified, and these and the collateral branches of the intrinsic neurons form a dense plexus whose individual fibres cross dendrites rather than lie parallel to them. Six cell types may also be distinguished with the electron microscope, and four of these can be correlated directly with those seen in Golgi impregnated material. Several kinds of dendrites are present, the commonest having numerous spines. Fewer spines are present on other varieties of dendrite, and those dendrites which are varicose have no spines. Numerous fine, nonmyelinated axons are present.

Recent findings on the afferent and efferent connexions of the striatum (the caudate nucleus and putamen) and globus pallidus have been summarized in an orderly sequence. The striatum receives afferent fibres from three main sources, the cerebral cortex, the intralaminar nuclei of the thalamus and the midbrain; the major features of each of these pathways are outlined. The striatum sends efferent fibres to the globus pallidus and the substantia nigra, and the two segments of the globus pallidus in turn project upon the subthalamic nucleus and upon the thalamus and midbrain tegmentum. Through the thalamus the major influence of the striopallidum is upon the motor area of the cerebral cortex, and it is suggested that through the midbrain tegmentum there may also be a descending influence upon the spinal cord. These findings from light microscopical investigations are synthesized with observations made in electron microscopic studies of the striatum and globus pallidus. On the basis of present knowledge of their structure and connexions attention is drawn to several marked similarities between these parts of the basal ganglia and the cerebellum.

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