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Schizophrenia, as a common mental disease, seriously threatens the physical and mental health of human beings. It is characterized by many mental and behavioral disorders, such as uncoordinated thinking and emotional mode which separated from the actual living environment. Patients with schizophrenia are prone to relapse and deterioration due to their long course of disease, resulting in the loss of labor force. It has been proved that the occurrence and development of schizophrenia is closely related to the abnormal development of oligodendrocytes, which have the function of myelin formation and the dysfunction of myelin sheath itself. For a comprehensive understanding of myelin abnormal effects on the pathogenesis of schizophrenia, this paper is to review the literature, then summarize and discuss the animal experimental literature related to the abnormal myelin sheath in schizophrenia from the perspectives of behavioristics, neuroimaging, protein expression and stereology, in order to further clarify the influence of the abnormal myelin sheath on the pathogenesis of schizophrenia and provide ideas for the diagnosis of schizophrenia and the research and development of new drugs. [ABSTRACT FROM AUTHOR]

Follow-up data are presented on a previously described child in whom myelinated nerve fibers presumably developed 5 1/2 months after an optic nerve decompression. During the subsequent five years, the myelinated nerve fibers have progressively enlarged. Five years after surgery, myelinated nerve fibers appeared in the patient's fellow eye. An additional two cases of documented acquired myelinated nerve fibers without any predisposing factors are reported. Myelinated nerve fibers can appear and progress after infancy.

Porton mice were used in the experiments. Pregnant animals were injected intravenously with a single dose of ethylnitrosourea (ENU). The poison was administered at the 15th day of pregnancy. The cerebral myelin of offsprings of the intoxicated mothers was examined with respect to the fatty acid spectrum of myelin lipids. The results obtained lead to the following conclusions: The fatty acid pattern of the individual myelin lipid fractions has revealed significant differences between the normal myelin and that isolated from brains of mice that had been subjected to transplacental intoxication by ENU. Transplacental intoxication by ENU has not only a carcinogenic effect on the central nervous system, but it obviously also affects the lipid metabolism of membraneous structures of the developing brain. ENU when acting during foetal life induces the formation of deviated myelin, that differs significantly with respect to its lipid and fatty acid composition from that of normally developing animals.

The central nervous system (CNS) findings associated with congenital hypomyelinating polyneuropathy (CHN) are not established due to a paucity of reported post-mortem examinations. In this report we describe the pathologic changes found in the peripheral nervous system and CNS in a 2 1/2-week-old infant with a clinical diagnosis of CHN who died of respiratory failure clinically attributed to phrenic nerve dysfunction. Macroscopic findings included striking hypoplasia of the corpus callosum and anterior commissure, cerebellum, crus cerebri, ventral pons and pyramids. Histologic and immunohistochemical findings included complete absence of myelin staining and myelin basic protein immunoreactivity (MBP-IR) in the cerebral hemispheres, cerebellum, brainstem, cranial nerves and spinal cord despite little or no detectable reduction in numbers of oligodendrocytes. A severe fibrillary astrocytosis was seen at each of these sites. A slight reduction in neurons was identified in the cerebellum and spinal cord but nowhere else in the brain. These findings raise the possibility that deficient or markedly delayed CNS myelination accompanies peripheral hypomyelination in some cases of CHN.

We describe a 37-week gestational age infant who presented with lethal arthrogryposis multiplex congenita due to complete absence of peripheral nervous system (PNS) myelin. Schwann cells accomplished successful developmental proliferation, migration, axonal ensheathment, basal lamina production, and subsequent cessation of proliferation, but failed in spiral lengthening and longitudinal growth. Internuclear distance was very short, resulting in marked Schwann cell hypercellularity. No supernumerary Schwann cells (onion bulbs) were found. No PNS myelin proteins (P0, P1, MAG) were detected by immunocytochemical methods, and the Schwann cells adopted many morphologic features characteristic of unmyelinated nerves. The defect appears to be an arrest in Schwann cell differentiation at the stages of mesaxon elongation and longitudinal growth.