The posterior portion of the corpus callosum is called the splenium; the anterior is called the genu (or "knee"); between the two is the truncus, the 'body' of the corpus callosum. The rostrum is the portion of the corpus callosum that projects posteriorly following from the anteriormost genu.
Thinner axons in the genu interconnect prefrontal cortex areas between the two sides of the brain. Those in the posterior body of the corpus callosum interconnect parietal lobe areas. Thicker axons in the midbody of the corpus callosum and in the splenium interconnect areas of the motor,somatosensory, and visual cortex.[1]
Using magnetic resonance diffusion tensor imaging, the studies of Hofer and Frahm [2] suggest that the anterior sixth of the corpus callosum interconnect the prefrontal parts of the brain; the next third, the premotor and supplementary motor regions; the following sixth, the motor areas; then the next twelfth deals with the sensory areas; and the final quarter, the parietal, temporal, and occipital lobes.
Pathology
- Alien hand syndrome
- A complete or partial absence of it in humans is called agenesis of the corpus callosum.
- Split-brain
- Septo-optic dysplasia (deMorsier syndrome)
- Alexia without agraphia (seen with damage to splenium of corpus callosum)
Split-brain is a lay term to describe the result when the corpus callosum connecting the two hemispheres of the brain is severed to some degree. The surgical operation to produce this condition is called corpus callosotomy and is usually used as a last resort to treat intractable epilepsy. Initially, partial callosotomies are performed; if this operation does not succeed, a complete callosotomy is performed to mitigate the risk of accidental physical injury by reducing the severity and violence of epileptic seizures. Prior to callosotomies, epilepsy is treated through pharmaceutical means.
A patient with a split brain, when shown an image in his or her left visual field (the left half of what both eyes take in, see optic tract), will be unable to vocally name what he or she has seen. This is because the speech-control center is in the left side of the brain in most people, and the image from the left visual field is sent only to the right side of the brain (those with the speech control center in the right side will experience similar symptoms when an image is presented in the right visual field). Since communication between the two sides of the brain is inhibited, the patient cannot name what the right side of the brain is seeing. The person can, however, pick up and show recognition of an object (one within the left overall visual field) with their left hand, since that hand is controlled by the right side of the brain.
The same effect occurs for visual pairs and reasoning. For example, a patient with split brain is shown a picture of a chicken and a snowy field in separate visual fields and asked to choose from a list of words the best association with the pictures. The patient would choose a chicken foot to associate with the chicken and a shovel to associate with the snow; however, when asked to reason why the patient chose the shovel, the response would relate to the chicken.
Alexia without agraphia is a form of alexia which almost always involves an infarct to the left posterior cerebral artery (which perfuses the splenium of the corpus callosum and left visual cortex, among other things).
The resulting deficit will be "Alexia without agraphia" - i.e., the patient can write but cannot read (even what they have just written). This is because the left visual cortex has been damaged, leaving only the right visual cortex (occipital lobe) able to process visual information, but it is unable to send this information to the language areas (Broca's area, Wernicke's area, etc) in the left brain because of the damage to the splenium of the corpus callosum.[1][2] The patient can still write because the pathways connecting the left-sided language areas to the motor areas are intact.[3]
It is also known as "Dejerine syndrome" (after Joseph Jules Dejerine, who described it in 1892[4]), but it should not be confused with medial medullary syndrome, which shares the same eponym.
Memory
In most tests, memory in either hemisphere of split-brained patients is generally lower than normal, though better than in patients with amnesia, suggesting that the forebrain commissures are important for the formation of some kinds of memory. It is suggested that posterior callosal sections which include the hippocampal commissures cause a mild memory deficit (in standardized free field testing) involving recognition[9].
[edit]Control
In general, split-brained patients behave in a coordinated, purposeful and consistent manner, despite the independent, parallel, usually different and occasionally conflicting processing of the same information from the environment by the two disconnected hemispheres. When two hemispheres receive competing stimuli at the same time, the response mode tends to determine which hemisphere controls behavior[10]. Often, split-brained patients are indistinguishable from normal adults. This is due to the compensatory phenomena; split-brained patients progressively acquire a variety of strategies to get around their interhemispheric transfer deficits.
[edit]Attention
Experiments on covert orienting of spatial attention using the Posner paradigm confirm the existence of two different attentional systems in the two hemispheres[11]. The right hemisphere was found superior to the left hemisphere on modified versions of spatial relations tests[12]. The components of mental imagery are differentially specialized: the right hemisphere was found superior for mental rotation[13], the left hemisphere superior for image generation[14].
Infarcts of the corpus callosum are not common and are attributed to a rich blood supply from three main arterial systems: the anterior communicating artery, the pericallosal artery, and the posterior pericallosal artery (4). A detailed description of the vascular supply to the corpus callosum was published by Ture et al (5), including variations in the main arterial supply. The pericallosal branch of the anterior cerebral artery is most often the main vascular supply to the body. The subcallosal and medial callosal arteries, branches of the anterior communicating artery, provide the main supply for the anterior portion of the corpus callosum. The posterior pericallosal artery, a branch of the posterior cerebral artery, supplies the splenium.
Chrysikopoulos et al (4) offer other possible explanations for the immunity of the corpus callosum to infarction. Isolatedinfarcts of the anterior and posterior cerebral arteries are uncommon, accounting for 12% of all infarcts, and when presentare found in conjunction with generalized atherosclerotic disease. All of the patients in our series had long histories of hypertension and three of the five patients had insulin-dependent diabetes mellitus, predisposing them to generalized atherosclerosis. Chrysikopoulos et al (4) note that the majority of strokes are thromboembolic in origin, and emboli tend to favor the middle cerebral artery distribution because of hemodynamic factors. Moreover, the penetrating vessels of the corpus callosum are small in size and generally run perpendicular to the parent artery, thus protecting the corpus callosum from emboli.
Kazui et al (6) found in their series that infarction localized to the anterior cerebral distribution was attributable mostcommonly to local atherothrombosis and occasionally to cardiogenic embolism. They also postulate that a hypoplastic A1 segment may facilitate the occurrence of embolism in the anterior cerebral artery distribution. MR angiography performed in one of the patients in our series (case 2) showed small anterior cerebral arteries relative to the other cerebral vessels. This was of uncertain etiology. Although stenosis was considered, no conventional angiogram was obtained.
Chrysikopoulos et al (4) found that the splenium of the corpus callosum was affected more often than was the body and genu. They attributed this to the greater incidence of posterior cerebral artery infarcts compared with anterior cerebral artery infarcts. In our series, all of the lesions involved the genu, body, or both, whereas none involved the splenium. The difference in the location of the infarcts in our study, as compared with that reported by Chrysikopoulos et al, may be due to the difference in the patient population; ie, patients with diabetes and hypertension develop generalized atherosclerosis, which in turn increases the incidence of anterior circulation infarction. Isolated anterior cerebral artery infarcts are rare, accounting for 0.6% of all cerebral infarcts (6). Chrysikopoulos et al (4) found evidence of hemorrhage in about 25% of their cases, whereas there was no evidence of hemorrhage in any of our cases. Thus, the presence of hemorrhage may suggest infarct, but the absence of hemorrhage should not exclude the diagnosis. Infarcts of the corpus callosum may exhibit a variable degree of mass effect. Mass effect is commonly seen in stroke, but when it occurs in a region such as the corpus callosum where stroke is often not considered, it suggests other entities that would require biopsy. Enhancement is often seen by the end of the 1st week and can persist for many weeks (7, 8). In many of our cases, the abnormal signal intensity or enhancement or both crossed the midline, unusual for infarct but not for tumor.
Clinically, infarcts of the corpus callosum are frequently associated with neuropsychiatric symptoms, mainly interhemispheric disconnection syndromes (9). In addition, specific syndromes such as dyspraxia contralateral to a paretic limb (10, 11) and alien hand syndrome (12, 13) have been reported, and an isolated gait disorder has been described in relation to lacunes in the anterior portion of the corpus callosum (12).
No comments:
Post a Comment