Corpus Callosum Damage Case Study

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AHSis a movement disorder characterized byinvoluntary and autonomous movements. AHS can be divided into threevariants, including the frontal, callosal and posterior AHSsubtypes (5,15). The callosal subtype is characterizedby intermanual conflict (antagonizing movements of the two hands),mostly due to the disconnection between the two cerebralhemispheres (16). The blood supplyto the corpus callosum is ample; thus, infraction in this area israre. The present study reports a case of callosal-subtype AHSpresenting following corpus callosum infarction. In addition, thecurrent case was compared with a collection of 31 previouslyreported cases of AHS that were caused by callosal infarction.

A 56-year-old woman presented at the YantaiYuhuangding Hospital (Yantai, China) in November 2011 withinvoluntary and autonomous activity of the right hand thatpersisted for 1 month, without apparent cause. Intermanual conflictwas the most troubling feature experienced. For instance, thepatient's right hand took off her clothing while she attempted todress with the left hand. The patient also reported weak right limband dysarthria. She had a history of hypertension, coronary arterydisease and type 2 diabetes mellitus, but no substance abusehistory, including smoking and drinking. No similar disease orsyndrome was reported for any family members. Written informedconsent was obtained from the patient.

Physical examination failed to revealed anepia,anarthria, autotopagnosia or apraxia. No signs of meningealirritation were observed. In addition, an ophthalmic examinationfailed to reveal any abnormalities, whereas a slightly superficialright nasolabial fold was detected. Muscle tension was normal, withlevel-5 muscle force in the right upper extremity and level-4 inthe right lower extremity (17).Sensory, finger-to-nose and left heel-knee-shin tests were normal.However, the heel-knee-shin test on the right side wasunsuccessful. Deep tendon reflex was normal, with no pathologicalsigns. The mini-mental state examination (MMSE) score was 30(18).

Doppler color imaging demonstrated atheroscleroticplaques in bilateral carotid arteries and increased resistance inbilateral vertebral arteries. Cranial magnetic resonance imaging(MRI) displayed long T1 and T2 signals, as well as high signals ondiffusion weighted imaging (DWI), in the body and splenium of theleft corpus callosum (Fig. 1). Brainmagnetic resonance angiography (MRA) 3 days following admissionrevealed extensive atherosclerosis and intermittent visualizationof the basilar artery (Fig. 2A).Cerebral digital subtraction angiography (DSA) of the right or leftinternal carotid artery showed the opening of the correspondingposterior communicating artery. Furthermore, bilateral posteriorcerebral arteries and basilar artery apex were visualized. The leftanterior cerebral artery and left pericallosal arteries appearedfaint. The right vertebral artery was narrow, and the distalsegment of the intracranial branch was occluded. In addition, theintracranial branch of the left vertebral artery and basilar arterywas significantly narrowed (Fig. 3).A diagnosis of callosal AHS was established based on theaforementioned observations. The characteristic features ofcallosal AHS reported in the present patient included involuntaryautonomous movement, and intermanual conflict. Infarction of thecorpus callosum was clearly demonstrated in MRI scans, while MRAand DSA revealed multiple lesions in the feeding arteries.

Frontal AHS is characterized by forced grasping ofobjects and impulsive reaching and groping movements toward nearbyobjects within the visual field. This type of AHS is typicallycaused by lesions located in the anterior corpus callosum, thesupplementary motor area, the anterior cingulate gyrus and themedial prefrontal cortex of the dominant hemisphere. By contrast,callosal AHS typically results from a callosal lesion and ischaracterized primarily by intermanual conflict and apraxia of thenon-dominant limb (5). Posterior AHSis characterized by the feeling of an alien hand and lefthemianesthesia, which lesions primarily in the cortex orsubcortical structures, such as the thalamus, parietal lobe andmedial temporal lobe that are supplied by the posterior cerebralartery (10,12,13,15). Thecurrent study reported a case with characteristic features ofcallosal AHS, including involuntary autonomous movement, as well asintermanual conflict. Infarction of the corpus callosum was clearlydemonstrated according to the imaging results.

In general, the literature search revealed that thelesion was complex in the majority (77.4%) of cases. Intermanualconflict was more common in simple corpus callosum infarctionpatients (85.7%), and grasp reflex was more frequently reported incomplex corpus callosum infarction patients (70.8%). Involuntarymasturbation seems to be unique to infarction of the right anteriorcorpus callosum (37,38). Table Ialso suggests that the right hemisphere is more frequentlyinvolved, since the right and left sides of the corpus callosumwere affected in 17 and 10 patients, respectively.

The corpus callosum is a fiber plate that conveysinformation between the two cerebral hemispheres (41). Callosal AHS putatively arises fromfailure in connection between the motor area and the supplementarymotor area in the two cerebral hemispheres (16,23).Damage to the corpus callosum may manifest as frontal or callosalAHS. Mixed AHS has been also reported following corpus callosuminfarction (24), in which thesymptoms include intermanual conflict (as in callosal AHS), feelingof an alien hand and hemianesthesia (as in posterior AHS thatinvolves the thalamus, parietal lobe or medial temporal lobe)(10,12,13,15).

Table I indicatesthat infarction of the corpus callosum typically occurs withlesions to other sites, including the medial frontal cortex,anterior cingulate gyrus and supplementary motor cortex. Similar tothe genu and body of the corpus callosum, these regions all receiveblood supply from the anterior cerebral artery. By contrast, thesplenium of the corpus callosum receives blood from the posteriorcerebral artery (42). Infarction atthe splenium of the corpus callosum is reportedly caused byembolism, whereas atherosclerotic cerebral infarction is the morecommon form of infarction in the genu and body of the corpuscallosum (43). The corpus callosumreceives blood supply from the anterior and the posterior cerebralarteries with extensive anastomosis, and thus is rarely affected byinfarction (42). In the presentcase, MRA and cerebral angiography revealed extensiveatherosclerosis throughout the intracranial vasculature, notably inthe left anterior cerebral and the vertebral basilar arteries.These imaging findings suggested the presence of atheroscleroticlesions in the anterior and posterior circulation.

AHS tends to be transient in patients with partialloss of the corpus callosum genu and splenium; in addition,patients with unilateral callosal lesions may regain connectivitybetween the two hemispheres if the remaining corpus callosum isfunctional (44). Permanent AHS maydevelop when the infarction involves two thirds of the anteriorcorpus callosum (45). Quickrecovery was noticed following antiplatelet therapy in the presentcase, suggesting that the remaining corpus callosum may havecompensated for the lesioned site, and that connectivity betweenthe bilateral cerebral hemispheres was re-established.

In conclusion, the present study reported aprototypic case of callosal AHS, which was apparently caused bycompromised anterior and posterior circulation. A notable issue inthis case is insufficient blood supply of the vertebra-basilararteries and the left anterior cerebral artery. This findinghighlights the need for comprehensive investigation of the cerebralvasculature in patients with AHS caused by infarction of the corpuscallosum.

Obstructive hydrocephalus with enlarged ventricles and outward bowing of the third ventricular recesses and elevation and thinning of the corpus callosum. The aqueduct is not definitely patent and may be the site of obstruction.

A right posterior VP shunt with valve has been inserted, the tip lies within the body of the right lateral ventricle. Ventricular size is enlarged, similar to the previous study. No acute intracranial hemorrhage. The basal cisterns are clear.

A right parietal shunt tube is seen with its tip within the trigone of the right lateral ventricle. No ventricular dilatation. Distorted appearance of the corpus callosum is noted with abnormal low T1 and high T2 and FLAIR signal involving the anterior part of the body. The posterior part of the body shows cystic changes of CSF-like signal. No diffusion restriction.

Hydrocephalus-related corpus callosum damage can occur in two patterns. In longstanding severe hydrocephalus, the corpus callosum gets impinged against the inferior free margin of the falx cerebri resulting in corpus callosum impingement syndrome.

The other pattern is callosal damage that occurs secondary to ventricular decompression of longstanding hydrocephalus, known as post-hydrocephalus corpus callosum damage. In this injury, the corpus callosum appears stretched but with no signal abnormalities before decompression and the signal changes start to develop only after shunt placement.

The importance of recognizing these patterns here is to differentiate these hydrocephalus-related callosal signal changes from the more serious conditions of transcallosal signal abnormalities such as lymphoma, glioblastoma, and demyelinating diseases.

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This paper reports the case of a 16-year-old man who had sustained a traumatic head injury. Neuroradiological examinations showed haemorrhagic lesion in corpus callosum. The patient initially demonstrated several symptoms of disconnection syndrome; however, these clinical signs later resolved in subtle dysfunctions that could be evidenced only by statistical analyses of performances to specific tests. It is thus suggested that comparable cases may be undetected by standard examination procedures.

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