Gender differences in the human cerebral cortex: more neurons in males; more processes in females.

This study's objective was to investigate morphometric gender differences of the cerebral cortex in six males and five females, 12 to 24 years old. Though human brains lack sexual dimorphism on routine neuropathologic examinations, gender-specific brain weight, functional, and morphologic differences exist, suggesting that cortical differences may be found. Yet the cerebral cortex may be exempt from gender differences, as demonstrated by the fact that normal males and females perform comparably on intelligence tests. Stereologic morphometry on standardized histologic sections from 30 bilateral cortical loci determined cortical thickness, neuronal density, and derived neuronal number estimates. The mean +/- SD cortical thickness of the 60 loci examined was similar in males and females with right and left hemispheric gender ratios being balanced. In contrast, the average neuronal density of the same 60 loci was significantly higher in the male group than in the female group, and the corresponding mean male-to-female ratios were 1.18 in the right and 1.13 in the left hemisphere, which differ significantly from each other and from the balanced cortical thickness ratios. Estimates of neuronal numbers -- the product of neuronal thickness times density -- were 13% higher in males than in females, with mean male-to-female ratios of 1.13 in both hemispheres. The data provide morphologic evidence of considerable cerebral cortical dimorphism with the demonstration of significantly higher neuronal densities and neuronal number estimates in males, though with similar mean cortical thickness, implying a reciprocal increase in neuropil/neuronal processes in the female cortex.

Human cortex development: estimates of neuronal numbers indicate major loss late during gestation.

This morphometric study explores temporal and topographic changes in the estimated neuronal number in human neocortex during the latter half of gestation and early infancy. Neuronal estimates are calculated from standardized measurements of cortical layer thickness and neuronal density in 6 neocortical regions in 9 human brains ranging from 17 weeks of gestation to 13 weeks postnatally. Layer thickness increases linearly with age while the average neuronal density first increases, then reaches a maximum at 20 weeks of gestation, and progressively declines. The sum of layer thickness times layer density estimates the number of neurons in a cortical column with a fixed surface area and a length that is equal to the cortical thickness. To derive an estimate of potentially overproduced neurons, the number of neurons in each cortical column was corrected for surface growth and for cortex gyration. These data show that a large percent of cortical neurons present at 20 weeks of gestation are used to populate the expanding cortex. Nevertheless, the growth-corrected data suggest that a substantial overproduction and secondary reduction of cortical neurons takes place mainly during the last quarter of gestation. The corrected mean number of neurons reaches a maximum at 28 weeks of gestation and then declines by approximately 70% to achieve a stable number of neurons around birth. This estimated number of neurons is significantly higher at 28 to 32 weeks of gestation than at 17 to 20 gestational weeks and at 0 to 13 postnatal weeks. These data imply that physiologic neuronal death (apoptosis) may play a major role in early human cortex development.

Pathology of the capsular and synovial hip nerves in chronic hip diseases.

Nerves of the synovial membrane and of the capsule of the hip have been studied with the usual techniques of optical neuropathology. We studied 52 hips from 46 patients: 13 hips of post-fracture states of the femoral neck, 13 hips of idiopathic osteonecrosis, 6 hips of rheumatoid arthritis, 6 hips of ankylosing spondylitis and 14 hips of osteoarthrosis. Small capsular and synovial nerves mainly located close to blood vessels are modified by the lesions of the surrounding tissue (inflammatory, vascular, traumatic and mechanical disturbances). The degree of involvement is related to the disease and its evolution. The peri- and endoneurium is thickened and demyelination is mostly observed. Nerve lesions begin focally and for some time are segmental. The final lesions correspond to a complete fibrous transformation of the nerve with loss of axons. We suggest a correlation between nerve lesions and the existence or absence of pain in the hip.

Paresis of lateral gaze alternating with so-called posterior internuclear ophthalmoplegia. A partial paramedian pontine reticular formation-abducens nucleus syndrome.

A patient with multiple myeloma developed gaze paresis to the left with slowed saccades and gaze-paretic nystagmus, which alternated with abduction palsy in the left eye (with preserved oculocephalic deviation) and dissociated adducting nystagmus in the right eye, suggesting so-called posterior internuclear ophthalmoplegia. At autopsy multiple small infarcts were found with partial destruction of the left paramedian pontine reticula formation (PPRF) extending towards the abducens nucleus, which was involved only in its inferior pole. The medial longitudinal fasciculus and other oculomotor structures were spared. It is suggested that slowing of all ipsilateral saccades with gaze-paretic nystagmus corresponded to partial destruction of the PPRF, and that intermitted abduction palsy in the ipsilateral eye with adduction nystagmus in the fellow eye was due to intermittant dysfunction of the abducens nucleus. Involvement of voluntary saccades, pursuit movements and vestibulo-ocular responses may be dissociated in partial lesions of the abducens nucleus.

Encephalopathy, peripheral neuropathy, dysautonomia, myasthenia gravis, malignant thymoma, and antiacetylcholine receptor antibodies in the CSF.

A 54-year-old man suffered from multiple neurologic disturbances (polyneuropathy, encephalopathy, dysautonomia) associated with myasthenia gravis and malignant thymoma. No morphological signs of inflammation were present in the brain and peripheral nerves. Antiacetylcholine receptor antibodies were present in the brain and peripheral nerves. Antiacetylcholine receptor antibodies were present in serum and in cerebrospinal fluid. The association of thymoma, myasthenia gravis, multiple neurologic syndromes, and antiacetylcholine receptor antibodies in serum and cerebrospinal fluid has not been reported as yet. We suggest that this clinical picture is related to a generalized cholinergic dysfunction.

Postnatal development of the visual cortex of the mouse after enucleation at birth.

Quantitative data in the neocortex up to the age of 180 days (neuronal densities, number of neurones, glial cells, dendritic intersections and spines) were compared in normal mice and mice enucleated at birth. Bilateral enucleation induced an increase of neuronal density in all cortical layers of areas 17, 18a, and 41, the supragranular layers II-III being more affected than layers IV-VI. This was noticed in layer II 10 days after the operation and was maximal in all layers between 30 and 60 days; at 180 days there was some return to normal of the neuronal density in all layers. The total number of neurones and glial cells were the same in the bilaterally enucleated mice as in the controls. No reaction in dendritic branching was evident for pyramids of layers III and V in areas 17 and 41 after bilateral enucleation. In contrast the number of spines was reduced on the apical dendrites of pyramids from layers II and V in area 17, but not in area 41. After unilateral enucleation the reaction was less severe and delayed compared with bilateral enucleation, the first signs of increase of neuronal density appearing 30 days after the lesion in the contralateral hemisphere. The contralateral areas 17 and 18a were more affected than the ipsilateral ones and area 41 showed no change compared to the control. As after bilateral enucleation, layers IV and V were least affected by unilateral enucleation in both ipsi- and contralateral cortices. These results suggest that deafferentation in an immature system affects the development of all cortical layers but with a greatest intensity in supragranular layers, which are not the main direct targets of thalamo-cortical input.

Analysis of 100 infant deaths with intraventricular hemorrhage: brain weights and risk factors.

Because the lowering of brain-tissue pressure is associated with a loss in brain weight, the brain weights of 100 infants with intraventricular hemorrhage were compared with those of 100 control infants. After the 30th week of gestation the brain weight of infants with intraventricular hemorrhage were lower than those of the controls. This finding supports the authors' hypothesis of a causal relationship between brain shrinkage and intraventricular hemorrhage. Of 13 other risk factors investigated, only prematurity could be related directly to the occurrence of intraventricular hemorrhage.

Intraventricular hemorrhage in premature infants: reappraisal and new hypothesis.

Germinal matrix hemorrhage leading to intraventricular hemorrhage results from an excessive pressure gradient between the blood-vessel lumen and the surrounding brain tissue. This gradient may be caused by increased intravascular pressure or--as this paper hypothesises--by decreased tissue pressure. Brain-tissue pressure depends on water content, and it decreases when water moves out of the brain, as occurs in conditions associated with dehydration, plasma hyperosmolality or hypotension. Such conditions occur frequently in premature infants, which may explain why intraventricular hemorrhage develops with a delay after birth. Its coincidence in time with postnatal head-shrinkage and its association with plasma hyperosmolality, hyperosmolar alkali therapy and hypotension strengthen the hypothesis of a cause and effect relationship between reduced cerebral tissue pressure and intraventricular hemorrhage.

Postnatal development of the dorsal lateral geniculate nucleus in the normal and enucleated albino mouse.

Quantitative data (numbers of neurones and glial cells, total volumes, internuclear volumes) were obtained during normal development and after bilateral and unilateral enucleation at birth in the dorsal lateral geniculate nucleus (LGNd) of the mouse, at 5, 10, 30, 60, and 180 days postnatal. During normal development there is a neuronal loss of about 30% up to 30 days, at which age the total number of neurones stabilises at around 17,000. Glial proliferation and an increase in the volume of LGNd continues at least to 180 days. More severe degenerative effects were found after bilateral than after unilateral enucleation. At 180 days, bilateral enucleation leads to a neuronal loss of 27% compared to the controls, with a glial deficit of 53% and a decrease in the volume of LGNd of 57%. Degenerative effects were very different in LGNd contralateral or ipsilateral to enucleation in monocularly enucleated mice, due to the extensive crossing of the retinal fibres. At 180 days, we found a deficit of 10% in the numbers of neurones and glial cells, in the ipsilateral LGNd compared to normal: the volume of LGNd was slightly less (3%) than in controls. The contralateral LGNd after unilateral enucleation behaved like LGNd after bilateral enucleation until 60 days. At 180 days, some minor modifications were found, showing an additional neuropil decrease of 13% and an additional neuronal loss of 6% in the bilaterally enucleated LGNd compared to the unilaterally enucleated contralateral LGNd. The time-course of degeneration both after bilateral and unilateral enucleation was discussed.

[Lesions of the nerves of the hip involving chronic rheumatic infections (ankylosing spondylitis, rheumatoid arthritis, arthrosis). Anatomopathologic study]. / Lésions des nerfs des hanches atteintes d'affections rhumatismales chroniques (spondylarthrite ankylosante, polyarthrite rhumatoïde, arthrose). Etude anatomo-pathologique.

We have studied the nerves of the synovium and capsules of 6 hips with ankylosing spondylitis, 6 hips with rheumatoid arthritis and 14 cases of coxarthrosis either primary or secondary to a malformation. The nerves were studied with the usual methods of peripheral neuropathology. In the various diseases except 5 cases of coxarthrosis secondary to a malformation, the inflammatory and vascular involvements with tissue fibrosis were able to affect the nerves crossing the tissues. This nerve involvement could be the cause of articular pain. Despite the importance of the surrounding lesions, the nerves are preserved for a long time and this could explain the persistance of the pain.

Long-term effects of postnatal undernutrition and maternal malnutrition on mouse cerebral cortex. II. Evolution of dendritic branchings and spines in the visual region.

Quantitative analysis of the dendritic branchings of pyramidal cells from layers V and III, as well as of the number of spines on their apical dendrites, were performed on the visual cortex of postnatally undernourished mice (2nd--21st day) and on that of pups from malnourished mothers (gestation and lactation). Animals were followed till 180 days of age after more than 5 months of nutritional rehabilitation, and data were obtained at 10, 15, 21, 30, 60, and 180 days of age. The increase and maturation of dendritic branchings and spines were much more reduced in postnatal undernutrition than in maternal malnutrition. Furthermore, permanent damage still remained at 180 days in postnatal undernutrition while almost no damage was statistically detectable after maternal malnutrition.

Long-term effects of postnatal undernutrition and maternal malnutrition on mouse cerebral cortex. I. Cellular densities, cortical volume and total numbers of cells.

Quantitative analysis of cellular densities as well as an estimate of the cortical volume and of its total cell population were performed on the cortex of postnatally undernourished mice (2--21 days) and on that of pups from malnourished mothers (gestation and lactation). Animals were followed until 180 days of age after more than 5 months of nutritional rehabilitation, and data were obtained at 10, 30, 60, and 180 days of age. The neuronal density was much higher in all cortical layers of the two experimental series, suggesting a delay in cortical maturation. Moreover, layers II, III, and IV were more delayed than layers I, V, and VI. Postnatal undernutrition had more severe effects than maternal malnutrition and the degree of recovery after a long rehabilitation was much less. The increase of the cortical volume was greatly reduced in postnatal undernutrition and to a lesser degree in maternal malnutrition. The total number of glial cells was also reduced more in postnatal undernutrition than in maternal malnutrition, but the total number of neurons was never smaller than in the controls.

[Selective neurectomies in hemifacial spasm: an anatomo-pathologic discovery]. / Neurectomies sélectives pour spasme hémifacial: une découverte anatomo-pathologique.

Today the treatment of choice in hemifacial palsy is selective neurectomy of the branches of the facial nerve. Palliative surgery has improved experience in the treatment of facial palsy. An anatomical finding is reported which could contribute to a better understanding of the etiology of facial spasm.

Postnatal development of the mouse cerebral neocortex. III. Some dynamical aspects.

In this paper we analyse our data from the quantitative cytoarchitectonic study of motor and sensory areas 10--4--3 and 2(Leuba and coll., 1977) and of visual and auditory area 5--17--18a--18--41 and 20 (Heumann and coll., 1977). The analysis of neuronal densities and cortical depths shows the following facts during the postnatal maturation: 1. Generally the sequence of maturation of the cortical layers is the same in the 9 studied areas: first layers I. and V, then VIb and VIa followed by III and IV and finally II. 2. This sequence is the same between 5 and 10 days as between 10 and 30 days. Still the maturation is much faster between 5 and 10 days. After 30 day differences between the layers are not very important. 3. For layers I, V and VI our 9 areas show an approximately similar degree of development from 5 days on. 4. Layers II, III and IV are in a faster period of development between 5 and 10 days. At this moment and for these layers, areas 17, 2, 3, 4 and 10 are less well developed than areas 41, 20, 18 and 18a. 5. One can thus consider that in mice the maturation of the areas seems to be more correlated with their localization than with their function. Effectively areas 41, 20 and 18a are in the vicinity of the rhinal fissure and a maturational gradient may start in this fissure. 6. In terms of neuronal densities and cortical depths an adult aspect of the layers and of the areas seems to be reached around 30 days. But some other phenomena of maturation exist after 30 days.

Postnatal development of the mouse cerebral neocortex. IV. Evolution of the total cortical volume, of the population of neurons and glial cells.

The total neocortical volume delimited between precise anatomical features was measured. Serial frontal sections cresyl-violet stained were measured with plainimetric methods and the total volume evaluated at 5, 10, 30, 60 and 180 days. The total volume was used to obtain the total number of neurons and glial cells at each age using our quantitative data (published in our previous papers). The evolution of the cellular densities were studied in the sensory and motor areas 10--4--3 and 2 (Leuba and coll. 1977) and in the visual and auditory areas 17--18a--18--41 and 20 (Heumann anc coll. 1977) in the mouse cerebral neocortex. 1. The total neocortical volume increases rapidly between 5 and 10 days, less between 10 and 30 days, slightly decreases at 60 days and reincreases at 180 days. 2. Between 5 and 30 days, the loss of cortical neurons is of about 30% by neuronal death. 3. The total number of glial cells doubles between 5 and 180 days. The increase is progressive through the development.

Cerebral coenurosis. Report of a case with arteritis.

A case of the unusual clinical condition of cerebral coenurosis, the unique parasitic disease that is localized only in the CNS, is reported. The patient had repeated attacks of transient hemiparesis due to intracranial arteritis which was demonstrated by several angiographic studies. The CSF showed a discreet lymphocytosis and increased immunoglobulins. This inflammatory reaction which preceeded the manifestations of the intracranial mass can be explained by the parasitic foreign bodies, the liberation of somatic and metabolic parasitic toxins and the immunological reaction of the organism. The arteritis of the basal intracranial vessels was probably secondary to the inflammatory reaction of the leptomeninges. In presence of the rare association of meningovascular disease and an expanding intracranial lesion a parasitic condition due to a larval stage of Cestodes (Hydatidosis, Cysticercosis, Coenurosis) should be always considered.