胼胝体压部可逆性病变的MRI诊断与临床分析

目的探讨胼胝体压部(splenium of the corpus callosum,SCC)可逆性病变的MRI表现及临床特点。方法回顾性分析8例脑MRI表现为单纯胼胝体压部可逆性病变患者的临床和影像学资料。结果 8例患者的SCC可逆性病变均为继发性,原发病分别为脑内感染5例,肝豆状核变性、低血糖脑病及脑外伤各1例。8例患者均急性起病,临床表现为发热、头痛5例,急性意识障碍2例,肌张力增高2例,颈强2例,均符合原发病的临床表现。8例均行脑MRI检查,均表现为T1低或等信号,T2及FLAIR序列高信号,DWI高信号(提示细胞源性水肿),其中4例行增强扫描未见强化。8例患者均于临床症状好转或消失后复查MRI提示病灶消失。结论 SCC可逆性病变在多种疾病中均可出现,无该病变相关的特异性临床表现,MRI表现提示病灶为细胞源性水肿可能。     

Neurons in the corpus callosum of the cat during postnatal development

The corpus callosum (CC) is a major telencephalic commissure containing mainly cortico-cortical axons and glial cells. We have identified neurons in the CC of the cat and quantified their number at different postnatal ages. An antibody against microtubule-associated protein 2 was used as a marker of neurons. Immunocytochemical double-labelling with neuron-specific enolase or gamma-aminobutyric acid antibodies in the absence of glial fibrillary acidic protein positivity confirmed the neuronal phenotype of these cells. CC neurons were also stained with anti-calbindin and anti-calretinin antibodies, typical for interneurons, and with an anti-neurofilament antibody, which in neocortex detects pyramidal neurons. Together, these findings suggest that the CC contains a mixed population of neuronal types. The quantification was corrected for double counting of adjacent sections and volume changes during CC development. Our data show that CC neurons are numerous early postnatally, and their number decreases with age. At birth, about 570 neurons are found within the CC boundaries and their number drops to about 200 in the adult. The distribution of the neurons within the CC also changes in development. Initially, many neurons are found throughout the CC, while at later ages they become restricted to the boundaries of the CC, and in the adult to the rostrum of the CC close to the septum pellucidum or to the indusium griseum. Although origin and function of transient CC neurons in development and in adulthood remain unknown, they are likely to be interstitial neurons. Some of them have well-developed and differentiated processes and resemble pyramidal cells or interneurons. An axon-guiding function during the early postnatal period can not be excluded.     

The existence of a separate, brief critical period for the corpus callosum to affect visual development

The critical period for the role of the corpus callosum in visual development was explored in terms of the length of time during which the callosum has any influence on the development of visual acuity. Cats were given a surgical section of the posterior corpus callosum at 1, 2, 3, 4 and 29 weeks of age. These, as well as normal and operated control cats, were behaviorally tested for visual acuity thresholds from 5 through 29 weeks of age. Only the 1, 2 and 3 week callosum-sectioned cats showed deficits in visual acuity; the 4 and 29 week callosum-sectioned cats had acuity thresholds equivalent to those of the control cats. These results define a relatively brief critical period of time during which the corpus callosum effectively interacts with the developing visual system. This critical period ends during the fourth postnatal week; throughout the first postnatal month the corpus callosum's effectiveness in altering subsequent visual development gradually declines. Using the amount of acuity deficit as the measure of alteration of visual development, the input of the corpus callosum during the first postnatal month is as critical to visual development as is normal visual input during the first 4-6 postnatal months.     

Myelination in the splenium of the corpus callosum in adult male and female rats

Previous work reported increases in the number of myelinated axons in the splenium of the rat corpus callosum between 25 and 60 days of age. In the present study, we quantified the area occupied by myelinated axons using a light microscopic point counting technique at 60, 120 and 180 days. Myelinated axons increased across these ages (p=0.001). Thus, myelination of the rat corpus callosum persists well into adulthood.     

Maturation of the corpus callosum of the rat: II. Influence of thyroid hormones on the number and maturation of axons

Quantitative electron microscopy has been used to study the number of callosal axons in the corpus callosum of normal and hypothyroid rats during postnatal development. At birth, the normal corpus callosum contains 4.4 x 10(6) axons. This number increases to 11.4 x 10(6) by 5 days of age (P5) and then, in contrast to cats and primates, remains constant until at least P60, the oldest age examined. The number of axons in the corpus callosum of hypothyroid animals is not significantly different from the values observed in normal rats at all ages studied, although the callosal axons of hypothyroid rats remain structurally immature. As extensive elimination of callosal axons has been shown to occur in normal rats past P5, we conclude that new callosal processes grow through the corpus callosum past this age that compensate numerically for the loss. Moreover, as the number of callosally projecting neurons seems to be higher in hypothyroid rats than in normal controls, it seems that the constant axon number derives from more parent neurons, and thus that there are more axon collaterals per callosal neuron in a normal animal than in a hypothyroid one. Taken together, these data indicate that although hypothyroidism does not alter the total number of callosally projecting axons, it interferes with the normal processes that define or sculpt the projection fields, thereby leading to a numerically normal projection with abnormal topography.     

Boomerang sign: Clinical significance of transient lesion in splenium of corpus callosum

Transient signal abnormality in the splenium of corpus callosum on magnetic resonance imaging (MRI) is occasionally encountered in clinical practice. It has been reported in various clinical conditions apart from patients with epilepsy. We describe 4 patients with different etiologies presenting with signal changes in the splenium of corpus callosum. They were diagnosed as having progressive myoclonic epilepsy (case 1), localization-related epilepsy (case 2), hemicrania continua (case 3), and postinfectious parkinsonism (case 4). While three patients had complete involvement of the splenium on diffusion-weighted image (“boomerang sign”), the patient having hemicrania continua showed semilunar involvement (“mini-boomerang”) on T2-weighted and FLAIR image. All the cases had noncontiguous involvement of the splenium. We herein, discuss these cases with transient splenial involvement and stress that such patients do not need aggressive diagnostic and therapeutic interventions. An attempt has been made to review the literature regarding the pathophysiology, etiology, and outcome of such lesions.     

Recovery of axonal myelination sheath and axonal caliber in the mouse corpus callosum following damage induced by N,N-diethyldithiocarbamate

Disulfiram is an aldehyde dehydrogenase inhibitor used for the treatment of alcohol dependence and of cocaine addiction. It has been demonstrated that subchronic administration of disulfiram or N,N-diethyldithiocarbamate (DEDTC), the main derivative of disulfiram, to rats can produce central-peripheral distal axonopathy. However, few data regarding the axonal effects of these compounds in the central nervous system exist. Our previous studies have revealed DEDTC-induced axonal damage in the mouse brain during the course of postnatal development, together with alterations in axonal pathfinding and in the myelination process, with partial recovery during the post-treatment period. In order to gather new data about how this axonal damage and recovery occurs in the central nervous system, we performed an ultrastructural analysis of the axons located in the corpus callosum from mice treated with DEDTC during postnatal development. The axonal caliber throughout the axonal area, the maximum axonal diameter, the maximum fiber diameter, and the axonal circularity, at different postnatal stages [from postnatal day (P)9 to P30], were analyzed. In addition, parameters related to the myelinization process (number of myelinated axons, sheath thickness, and the ratio of myelinated axons to total axons) were evaluated. A reduction in the average value of axonal caliber during treatment and a delay in the axonal myelination process were detected. Whereas early recovery of individual axons occurred after treatment (P22), complete recovery of myelinated axons occurred at late postnatal stages (P42). Therefore, chronic treatment with dithiocarbamates requires periods of rest to encourage the recovery of myelinated axons.     

Transient lesions of the splenium of the corpus callosum following rapid withdrawal of levetiracetam

Transient lesions of the splenium of the corpus callosum are characterized by MRI findings. The lesions are very rare, but significant from a clinical standpoint as differential diagnoses include serious conditions such as encephalitis, meningitis, and neuroleptic malignant syndrome. In addition, it is reported that some are attributed to the withdrawal of antiepileptic drugs. Here, we present a case of transient lesions of the splenium of the corpus callosum following rapid withdrawal of levetiracetam alone. To the best of our knowledge, this is the first report of such a case. Moreover, it is reported that cases of incidental transient lesions of the splenium of the corpus callosum are detected in Japan more often than in other countries, and as a result are prone to over‐triage. Taking this into consideration, in the event of transient lesions of the splenium of the corpus callosum, the utmost attention must be paid to clinical symptoms and history relating to any of the aforementioned serious conditions.     

A case of prosopometamorphopsia caused by infarction of the splenium of the corpus callosum and major forceps

ABSTRACT

An adult female complained of enlargement of right eyes in other people. Diffusion-weighted imaging detected an abnormal high-intensity area in the region from the splenium of the corpus callosum to the major forceps on the right side. The patient reported that right eyes appeared larger in size, which suggested prosopometamorphopsia. Adichotic listening test identified left-ear deficit. Acombination of prosopometamorphopsia and left-ear deficit was not identified in the reported patients. Prosopometamorphopsia in most of the reported patients included the eye as did that in our patient. This result suggested the importance of information on the eye in recognizing faces.     

Deafferentation and axotomy of neurons in cat striate cortex: Time course of changes in binocularity following corpus callosum transection

Single neurons were recorded in the callosal terminal and cell zones of area 17 in the cat to assess the time course of changes in the proportion of binocular neurons produced by corpus callosum transection. The callosal terminal zone contains all the degenerating terminals in area 17 after corpus callosum transection. The callosal cell zone contains all the cells in area 17 which contribute axons to the corpus callosum. The cell zone is larger than, and partially overlaps, the callosal terminal zone. After corpus callosum transection there was an initial change in ocular dominance of neurons in both callosal zones. This initial change was followed by a reduction in the proportion of binocular neurons in both zones. This reduction became maximal 2–4 weeks after transection. In the callosal terminal zone, binocularity did not recover even at the longest postoperative periods examined (31–42 weeks). In the part of the callosal cell zone outside of the callosal terminal zone, the proportion of binocular neurons began to recover after 5 weeks and was at normal levels at the longest survival periods studied. Corpus callosum transection deafferents and axotomizes cells in the callosal terminal zone and, since central neurons do not regenerate their long-ranging axons, the combined effects of deafferentation and axotomy in this zone are permanent. The callosal cell zone outside of the callosal terminal zone contains axotomized cells and no degenerating terminals following transection. The recovery of binocularity in this region may be attributed to the transient changes which axotomized cells undergo. The zone which contains no callosal cells or terminals is unaffected by transection of the corpus callosum.     

Reversible demyelinisation of corpus callosum in the course of Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of an unknown aetiology that is marked by focal demyelinisation in the corpus callosum. Chronic alcohol abuse plays an important role in its development. Its course is unfavourable, although rare cases of clinical improvement confirmed in MRI have been reported. Until now, no case of Marchiafava-Bignami disease diagnosed intra vitam was so far described on the territory of Poland. The authors present such a case with favourable course. A 52-year-old male with chronic alcoholism was hospitalised due to altered consciousness which developed subacutely prior to admission. The first MRI scans yielded demyelinating lesions in the corpus callosum. The clinical and radiological findings were consistent with the diagnosis of Marchiafava-Bignami disease. Thiamine, vitamin B12, folic acid and amantadine were administered, which resulted in an improvement in both motor and cognitive functions. Control MRI scans revealed remyelinisation of the corpus callosum. Hence, this technique proved itself to be useful in monitoring the course of the disease.     

Somatosensory receptive fields of fibres in the rostral corpus callosum of the cat

The corpus callosum is the principal neocortical commissure which transmits lateralized information between the hemispheres. The aim of the present experiment was to study the receptive field (RF) properties of somatosensory callosal fibres in the cat. The callosum was approached under direct visual control and axonic responses were recorded under N2O anaesthesia using tungsten microelectrodes or, mostly, glass micropipettes. RFs representing all the sensory submodalities tested (light touch, medium and deep pressure, joint movement and light pinches) were found to be present in the axons which travelled through the callosum. Rapidly adapting units were more common than slowly adapting ones. The axial and para-axial portions of the body accounted for about three-fifths of all RFs, followed by the head (about one-fifth), with the rest responding to stimulation of the extremities. The medial borders of most of the unilateral RFs situated on the trunk and, to a lesser degree, the head, extended to the mid-line. The results are interpreted in terms of the roles of the corpus callosum in mid-line fusion and interhemispheric transfer.     

Developmental changes in the heavy subunit of neurofilaments in the corpus callosum of the cat

In the corpus callosum of the cat, the heavy subunit of neurofilaments (NFH) can be demonstrated with the monoclonal antibody NE14, as early as P11, not at P3, and only in a few axons. At P18-19 and more markedly at P29, many more callosal axons have become positive to NE14 and this is similar to what is found in the adult. In contrast, callosal axons become positive to the neurofilament antibody SMI-32 only between P29 and P39 and remain positive in the adult. Treatment with alkaline phosphatase prevents axonal staining with NE14, but results in SMI-32 staining of a few callosal axons as early as P11, but not at P3. Between P11 and P19 the number of axons stained with SMI-32 after alkaline phosphatase treatment increases, in parallel with that of axons stained with NE14. Thus NE14 appears to recognize a phosphorylated form of NFH, while SMI-32 appears to recognize an epitope of NFH which is either masked by phosphate or inaccessible until between P29 and P39, unless the tissue is treated with alkaline phosphatase. These two forms of NFH appear towards the end of the period of massive developmental elimination of callosal axons. They are also synchronous with changes in the spacing of neurofilaments quantified in a separate ultrastructural study. These cytoskeletal changes may terminate the juvenile-labile state of callosal axons and allow further axial growth of the axon.