Heterotopic Purkinje cells are found in the superficial cerebellar cortex in various microscopic sections of the cerebellum of adult representatives of the mammalian orders including insectivores, rodents, carnivores, artio- dactyls and primates, as well as normal and pathological human beings of different ages. Superficial to the middle layer of the cerebellar cortex the heterotopic Purkinje cells are hung on the outermost margin of the cortex or even slipped into the subpial space. Within the molecular layer they subsist in isolation, in groups, in rarefied file, in tortuous alignment, or in wholesale displacement. The heterotopic Purkinje cells are largely hypotrophic with roundish bodies, large nuclei, little cytoplasm, and slender and straight dendrites. Their orientation is multifarious. They are, again, often pathological, being elongated, withered, or with multiple nuclei or nucleoli. They are frequently accompanied by primitive granules which geneti- cally descend from the superficial to the deep planes, thus hinting at their common source. The theory of ventrieular origin fails to explain the aberration of the Purkinje cells to the superficial parts, whereas the facts of heterotopy reflect their origination from the margin and their descent towards the middle level as products of a secondary germination. Under adverse conditions, the primordial Purkinje cells are affected in their capacity of migration and differentiation and, consequently, remain in the original ger- minal bed or slip into the subpial cavity with the crumpling pia mater. They may, again, halt midway singly, collectively, in interrupted file, in sinuous row formation, or in dispersion throughout the whole molecular layer. Cortical patches occasionally present in the interior of pathological cerebellum testifies to the capacity of the potential germinal cells coming from the ventricular matrix to proliferate Purkinje and other cortical cells in the deep as well as in the superficial portions. The retention at adult age of the 'external' granular or Kirschhof's layer together with simulta- neous reduction or absence of Purkinje cells below implies the derivation of the latter cells normally from the margin through a stage corresponding to such granules. The heterotopy of Purkinje cells in the superficial cortex signifies that a part (if not whole) of them at least originate from the marginal granular layer of the early stage.

The lumbosacral segments of 12 spinal cords of normal new-borns and adults(Figs.1—3),and of sympodic (Figs.4—5) and diplomyeliac (Fig.6) fetuses were prepared for a microscopicstudy with special reference to the condition of the posteromedial cell column (pm).Apart fromthe 2 or 3 doubtful cases,this cell column is definitely present,which spreads dorsally and meetsits fellow across the midline in front of the central canal (cc),at S4 thus constituting a commissuralnucleus (ncs).This column possibly participates in the innervation of the pelvic and perinealmuscles which are attached to the midplane.

The lumbosacral cord of a 55-day baby girl was cut serially and stained for a microscopicstudy.It was twice split into two with extensive dysplasia in its dorsal parts.Numerous primarysensory cells were strewn within the cord.The present study was particularly concerned with theirclassification,distribution and derivation.In addition to their normal sites,the sensory ganglionic cells are scattered on the dorsal aspectsof the cord,along the space between the separated cords,in the openings of the anterior and posteriormedian fissures and also within the crevices inside the cord,yet communicating to the outside.Such sensory elements are surrounded with capsular cells;this is also characteristic of a few sen-sory cells slightly sunken into the intramedullary structures in continuation with the heterotopicganglionic formations.A number of the sensory cells are deeply embedded in the supernumerary gray and white for-mations chiefly in the dorsal portions;they are especially numerous in the anterior gray commissureand the anterior horn.Such cells are devoid of a capsule.In the early embryonic period,unfavorable conditions retard the mutual approximation of theneural folds and the precocious ectomesenchyme thrusts itself between them.The dorsal edges ofthe folds are then forced to bend ventrally toward the neural plate,resulting in a duplication of thespinal cord.During the rolling-in process,the irregular margins of the neural folds and the out-thrusts ofthe ectomesenchyme conjoin to produce the supernumeraray structures in the dorsal portions of thecord.Some presumptive sensory elements on the folds may be roiled into such intramedullary unitsand grow up in situ.The neural crest represents the spear-head of the rollingin fold;its presumptive sensory ele-ments may well disperse themselves into the precursory anterior gray commissure and theanterior horn.The primarys sensory cells and the capsular cells are both derived from the ectoderm.Theformer bear capsular cells in case they have participated in the process of ganglion formation;whereas they lack such a capsule if they grow up right in their erratic sites.The intraspinal sensory ganglionic cells are chiefly derived from the neural crest;this doesnot exclude the tube wall as being another possible source.Though erratic in postion,the intraspinal sensory cells may perform a fairly normal function.

Thirteen adult guinea-pigs were divided into 3 groups:2 as normal controls;6 and 5 being treated with streptomycin sulphate 200 and 400mg per kilo body weight res- pectively for 21—60 days.The vestibular and auditory functions were tested.Their brains were prepared for Bielschowsky and Nissl sections.Microscopic examination re- vealed the following facts. Vascular disturbances prevail in the nervous system.The blood vessels are crumpled with concommittent perivascular edema.The adjacent nervous tissue shows ischemic softening and the nerve fibres become demyelinated. The intoxicated nerve cells are generally dehydrated and shrunken often with eccen- tricity of nuclei and chromophilic lumps.Gliosis and neurophagosis are common. The vestibular and cochlear systems of the eighth or stato-acoustic nerve exhibit intoxicative changes in the 2 groups of animals.On the peripheral as well as the central side,the degeneration of the vestibular structures supercedes that of the cochlear system. The site and nature of the intoxication are much alike in the light and heavy-dose groups,yet the latter shows a higher severity. The degenerative alterations appear simultaneously in the perpheral and central struc- tures.A question of primacy in intoxication—peripheral or central—is not existent. There is a chain of structures on the peripheral and central sides of the stato-acoustic system;their degeneration does not proceed along the conduction path,nor the degree of intoxication varies with their relative positions on the conduction scale.The peri- pheral and central units get intoxicated independently. Besides the stato-acoustic structures streptomycin afflicts other sensory(e.g.trige- minal) and motor systems,the viscero-motor in particular.Streptomycin intoxication is general in nature,yet some structures are especially sensitive to it. The relative vulnerability to streptomycin of the nervous structures is apparently conditioned by their chemical constitution. Streptomycin injuries higher brain parts which are mainly motor,especially viscero- motor.The diencephalic viscero-motor nuclei,the striate complex and the visceral cor- tex are excessively disintegrated.The extensive intoxicative manifestations have a neurological basis. The toxin of streptomycin affects the entire nervous system and hence the whole bodily mechanisms.Its medical application calls for a meticulous consideration with respect to the patient's sensitivity to the antibiotic,the size of the dose and the length of the therapeutic course.

This report deals with the brain and spinal cord of a porencephalic nursling of 8months. Intermittent serial colloidin sections were cut and stained by Nissl and Weiltechniques. The left cerebral hemisphere is smaller with deeper sulci and narrower gyri. Theinsular lobe is non-existent; and the frontal parietal and temporal opercula are all miss-ing. A cavity underlies this region and communicates with the lateral ventricle beingcovered Iaterally by a thickened membrane about 4?0.8 cm in area. Most of the front-al, parietal and temporal lobes and the whole occipital lobe are present. The left pyramidal tract is undeveloped. Compensatory hypertrophy is shown byvarious central structures such as the right pyramidal tract (together with the aberrantpyramidal bundles), and the extrapyramidal gray masses-lenticular, caudate and sub-thalamic nuclei and substantia nigra. In the cerebellar system, the brachium conjunc-tivum on the left side and the red nucleus and the inferior olivary nucleus on the rightare over-developed. Other hypertrophied structures include the left gracile and cuneatenuclei, the right lemniscus medialis, together with the anterior funiculus, posterior hornand the nucleus dorsalis in the right half of the spinal cord. The postnatal heightened use of bodily organs naturally induces an over-developmentof, besides others, the central structure. With a short life-span and retarded develop-ment, the present case had a too limited activity to influence the size of its central or-gans. Moreover, a number of central nuclear masses manifest a compensatory enlarge-ment, thus indicating a heightened mitotic activity of the nerve cells in the embryonicperiod. This hypertrophy is, them, largely prenatal. The current theories of compensation such as self-regulation, substitution and trans-fer of functions, are not explanatory and, thus, unsatisfactory. Behind such concepts,there shou1d exist a more fundamental and yet unspecified factor of growth. The pre-sent study has demonstrated more facts of compensatory development than the previousauthors. As to the theories of compensation, it is better to reserve a definite judgement.