A novel categorization of the muscular branches of the tibial nerve within the popliteal fossa.

BACKGROUND: The muscular branches of the tibial nerve within the popliteal fossa innervate the gastrocnemius, soleus, plantaris, and popliteus muscles. Various branching patterns have been described in textbooks; however, the underlying fundamental rules explaining the patterns remain unclear. Understanding the fundamental rule explaining the branching pattern of the innervating nerves is essential for understanding the ontogeny of skeletal muscles. Therefore, this study aimed at establishing a theory to explain the branching pattern of the muscular branches of the tibial nerve within the popliteal fossa. METHODS: The branching patterns of the muscular branches of the tibial nerve within the popliteal fossa were examined macroscopically in 62 lower limbs derived from 31 adult cadavers (22 males and 9 females, aged 49-95 years). RESULTS: The branch to the medial head of the gastrocnemius muscle invariably arose from the posteromedial side of the tibial nerve. The branches to the soleus muscle and lateral head of the gastrocnemius muscle had a common trunk in all the lower limbs and invariably arose from the posterolateral side. The branches to the plantaris and popliteus muscles arose anteriorly from the tibial nerve in this order (plantaris branch first, followed by the popliteus branch). These branches invariably arose more distally than the branch to both the heads of the gastrocnemius and soleus muscles. CONCLUSIONS: Based on these fundamental branching patterns, we suggest a novel branching categorization. The branches could be categorized into a posterior group and an anterior group, which has independent branches to the plantaris and popliteus muscles. This fundamental branching pattern and novel categorization contribute to the understanding of the ontogeny of the skeletal muscles around the flexor compartment of the leg.

Effect of preconditioning on propofol-induced neurotoxicity during the developmental period.

At therapeutic concentrations, propofol (PPF), an anesthetic agent, significantly elevates intracellular calcium concentration ([Ca2 +]i) and induces neural death during the developmental period. Preconditioning enables specialized tissues to tolerate major insults better compared with tissues that have already been exposed to sublethal insults. Here, we investigated whether the neurotoxicity induced by clinical concentrations of PPF could be alleviated by prior exposure to sublethal amounts of PPF. Cortical neurons from embryonic day (E) 17 Wistar rat fetuses were cultured in vitro, and on day in vitro (DIV) 2, the cells were preconditioned by exposure to PPF (PPF-PC) at either 100 nM or 1 µM for 24 h. For morphological observations, cells were exposed to clinical concentrations of PPF (10 µM or 100 µM) for 24 h and the survival ratio (SR) was calculated. Calcium imaging revealed significant PPF-induced [Ca2+]i elevation in cells on DIV 4 regardless of PPF-PC. Additionally, PPF-PC did not alleviate neural cell death induced by PPF under any condition. Our findings indicate that PPF-PC does not alleviate PPF-induced neurotoxicity during the developmental period.

A bilateral third head of the gastrocnemius which is morphologically similar to the plantaris.

PURPOSE: An extra muscle was observed on both sides of the popliteal fossa in the cadaver of a 78-year-old Japanese male during dissection. The aim of this case report was to identify whether this variant is a double plantaris or a third head of the gastrocnemius according to its morphological characteristics and innervation. METHODS: The muscles were displayed by careful dissection and delineation of surrounding structures. The size of each of the muscle bellies and tendons of those extra muscles were measured manually by the vernier caliper. RESULTS: The origin of each extra muscle was lateral to the tibial nerve and superior to the plantaris, and each extra muscle which transitioned to a descending tendon parallel to the plantaris had a cone-shaped belly. However, the tendon of the extra muscles was fused into the investing fascia of the gastrocnemius with a tendon length of 4.5 cm on the left and 4.6 cm on the right. The extra muscles were innervated by the branch of the tibial nerve to the medial head of the gastrocnemius on both sides. CONCLUSION: Although they had an origin and shape similar to that of the plantaris, we identified the extra muscles in this case as a third head of the gastrocnemius, because of innervation to the plantaris arises directly from the tibial nerve. This case highlighted that the innervation is essential to understanding the myogenesis of extra muscles, especially in cases which are difficult to categorize based on the morphological features of the muscle.

Intravenous anesthetic-induced calcium dysregulation and neurotoxic shift with age during development in primary cultured neurons.

Anesthetic-induced neurotoxicity in the developing brain is a concern. This neurotoxicity is closely related to anesthetic exposure time, dose, and developmental stages. Using calcium imaging and morphological examinations in vitro, we sought to determine whether intravenous anesthetic-induced direct neurotoxicity varies according to different stages of the days in vitro (DIV) of neurons in primary culture. Cortical neurons from E17 Wistar rats were prepared. On DIV 3, 7, and 13, cells were exposed to the intravenous anesthetics thiopental sodium (TPS), midazolam (MDZ), or propofol (PPF), to investigate direct neurotoxicity using morphological experiments. Furthermore, using calcium imaging, the anesthetic-induced intracellular calcium concentration ([Ca2+]i) elevation was monitored in cells on DIV 4, 8, and 13. All anesthetics elicited significant [Ca2+]i increases on DIV 4. While TPS (100 µM) and MDZ (10 µM) did not alter neuronal death, PPF (10 µM and 100 µM) decreased the survival ratio (SR) significantly. On DIV 8, TPS and MDZ did not elicit [Ca2+]i elevation or SR decrease, while PPF still induced [Ca2+]i elevation (both at 10 µM and 100 µM) and significant SR decrease at 100 µM (0.76 ± 0.03; P < 0.05), but not at 10 µM (0.91 ± 0.03). Such anesthetic-induced [Ca2+]i elevation and SR decrease were not observed on DIV 13-14 for any of the anesthetic drugs. Our study indicates that more caution may be exercised when using PPF compared to TPS or MDZ during development.

Enhancement of Lymphatic Vessels in the Superficial Layer in a Rat Model of a Lymphedematous Response.

BACKGROUND: The morphologic and histologic behavior of lymphatic vessels in lymphedema has not been well analyzed using laboratory animals. The purpose of the present study was to elucidate the regeneration process of lymphatic vessels after acute lymphedema in a rat model. METHODS: The acute lymphedema was induced by an amputation and a replantation surgery on a rat hind limb. Recovery of lymphatic flow was traced using fluorescent lymphography with dye injection. The morphology and number of lymphatic vessels were immunohistochemically detected and quantified in both superficial and deep layers. RESULTS: The swelling was the most severe, and the number of lymphatic vessels in the superficial layer was significantly and maximally increased on postoperative day 3. Backflows and overflows were also detectable in the superficial layer on postoperative day 3. The number of lymphatic vessels had decreased but remained significantly higher than that in the controls on postoperative day 14, when the swelling decreased to the levels in the controls. In contrast, the number of lymphatic vessels in the deep layer showed a tendency toward increased numbers; however, it was not statistically significant on postoperative day 3, 7, or 14. CONCLUSIONS: We have obtained solid evidence showing the differential potency of lymphatic vessels between the superficial and the deep layers after temporal lymphedematous induction. Further analysis of lymphedematous responses in animal models could provide new insights into the challenges associated with the clinical treatment of lymphedema.

Positive association between the cross-sectional area of the rhomboid muscle, and the range of shoulder abduction after neck dissection surgery.

OBJECTIVE: To evaluate the association between the cross-sectional area of selected shoulder and scapular muscles and the range of shoulder abduction, early after neck dissection surgery. PATIENTS AND METHODS: Twenty-seven patients (contributing 34 upper limbs), who had undergone neck dissection surgery for head and neck malignancy, were enrolled into the study. Loss of strength of the trapezius muscle at 1-month post-surgery was quantified by the change in active range of shoulder abduction (%A-ROM), measured by hand-held goniometry in a standing position, from baseline, before surgery. The cross-sectional area of the following muscles were measured on unenhanced computed tomography images after surgery: trapezius, rhomboid, serratus anterior, pectoralis major, deltoid, and biceps brachii. RESULTS: There was a significant positive correlation between the %A-ROM and the cross-sectional area of the rhomboid muscle. CONCLUSION: Greater active shoulder abduction early after surgery is associated with a greater cross-sectional area of the rhomboid muscle. This muscle should be included in intensive programs for rehabilitation of upper limb movement after neck dissection surgery.

Responses of Korean physical therapy students after practice with a virtual anatomical system in Japan.

[Purpose] To investigate responses of Korean physical therapy students, receiving medical terminology education in physical therapy both in Korean and English, after practice with a virtual anatomical system. [Subjects and Methods] The participants were 25 physical therapy students from Konyang University in South Korea visiting the International University of Health and Welfare for training purposes. The virtual anatomy practice was conducted in English using 3 dimensional virtual anatomy software constructed using real cadaver photographs. A questionnaire about this practice and anatomy was completed after the practice. [Results] The results of the questionnaire showed a trend toward high scores for virtual anatomy practice. [Conclusion] The present virtual anatomy system was created using multi-directional photographs from a real cadaver; therefore, it can be used as an auxiliary means of education using cadavers.

Microstructural Differences in the Corpus Callosum in Patients With Bipolar Disorder and Major Depressive Disorder.

OBJECTIVE: It is difficult to distinguish between bipolar disorder and major depressive disorder (MDD) in patients lacking a clear history of mania. There is an urgent need for an objective biomarker for differential diagnosis. Using diffusion tensor imaging, this study investigated the differences in the brain white matter microstructure between patients with bipolar disorder and MDD. METHODS: Participants included 16 patients with bipolar disorder and 23 patients with MDD having depressed or euthymic states based on DSM-IV-TR criteria and 23 healthy volunteers. Whole-brain voxel-based morphometric analysis was used to detect any significant differences in fractional anisotropy between patients with bipolar disorder and MDD. The study was conducted between August 2011 and July 2015. RESULTS: We found a significant decrease in fractional anisotropy values in the anterior part of the corpus callosum in patients with bipolar disorder compared with MDD (P < .001), which did not depend on the patients' affective state. This decrease was associated with increased radial diffusivity values (P < .05), which was also found in patients with bipolar disorder when compared with healthy volunteers (P < .05). We predicted bipolar disorder and MDD in all patients using the fractional anisotropy values, with a correct classification rate of 76.9%. CONCLUSIONS: The present study revealed that patients with bipolar disorder have microstructural abnormalities in the corpus callosum during depressed or euthymic states, which may deteriorate the exchange of emotional information between the cerebral hemispheres, resulting in emotional dysregulation. Our results indicate the possible use of diffusion tensor imaging as a differential diagnostic tool.

Test-retest reproducibility of extrastriatal binding with 123I-FP-CIT SPECT in healthy male subjects.

123I-labeled 2ß-carbomethoxy-3ß-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123I-FP-CIT) is used to assess striatal dopamine transporter (DAT) expression, but it can also quantify extrastriatal serotonin transporter (SERT) expressions. While FP-CIT uptake in extrastriatal regions has been quantified, no information exists on the reproducibility of the 123I-FP-CIT specific uptake ratio (SUR) in extrastriatal regions. We investigated test-retest reproducibility of 123I-FP-CIT binding in the striatum, the midbrain, and cortical regions in eight healthy male subjects. All subjects underwent two 123I-FP-CIT SPECT scans, and SUR was calculated using the cerebellum as the reference. We found good test-retest reproducibility of 123I-FP-CIT SUR in the midbrain, and in the lateral frontal/temporal cortex and combined cortical regions. The overall variability and intraclass correlation of SUR were, respectively, 4.9-7.8% and 0.90-0.96 in striatal regions, 8.6% and 0.79 in the midbrain, and 3.6-9.1% and 0.84-0.95 in the lateral frontal/temporal cortex and combined cortical regions. Our results provide evidence that 123I-FP-CIT SPECT is a valid technique for analyzing striatal DAT, as well as extrastriatal SERT in areas such as the SERT-enriched midbrain. In addition, our data suggest that 123I-FP-CIT could be used for analyzing SERT in regions with relatively low SERT expression (e.g., temporal or frontal cortices).

Thiopental sodium preserves the responsiveness to glutamate but not acetylcholine in rat primary cultured neurons exposed to hypoxia.

Although many in vitro studies demonstrated that thiopental sodium (TPS) is a promising neuroprotective agent, clinical attempts to use TPS showed mainly unsatisfactory results. We investigated the neuroprotective effects of TPS against hypoxic insults (HI), and the responses of the neurons to l-glutamate and acetylcholine application. Neurons prepared from E17 Wistar rats were used after 2weeks in culture. The neurons were exposed to 12-h HI with or without TPS. HI-induced neurotoxicity was evaluated morphologically. Moreover, we investigated the dynamics of the free intracellular calcium ([Ca(2+)]i) in the surviving neurons after HI with or without TPS pretreatment following the application of neurotransmitters. TPS was neuroprotective against HI according to the morphological examinations (0.73±0.06 vs. 0.52±0.07, P=0.04). While the response to l-glutamate was maintained (0.89±0.08 vs. 1.02±0.09, P=0.60), the [Ca(2+)]i response to acetylcholine was notably impaired (0.59±0.02 vs. 0.94±0.04, P<0.01). Though TPS to cortical cultures was neuroprotective against HI morphologically, the [Ca(2+)]i response not to l-glutamate but to acetylcholine was impaired. This may partially explain the inconsistent results regarding the neuroprotective effects of TPS between experimental studies and clinical settings.

Comparative morphology and development of extra-ocular muscles in the lamprey and gnathostomes reveal the ancestral state and developmental patterns of the vertebrate head.

The ancestral configuration of the vertebrate head has long been an intriguing topic in comparative morphology and evolutionary biology. One peculiar component of the vertebrate head is the presence of extra-ocular muscles (EOMs), the developmental mechanism and evolution of which remain to be determined. The head mesoderm of elasmobranchs undergoes local epithelialization into three head cavities, precursors of the EOMs. In contrast, in avians, these muscles appear to develop mainly from the mesenchymal head mesoderm. Importantly, in the basal vertebrate lamprey, the head mesoderm does not show overt head cavities or signs of segmental boundaries, and the development of the EOMs is not well described. Furthermore, the disposition of the lamprey EOMs differs from those the rest of vertebrates, in which the morphological pattern of EOMs is strongly conserved. To better understand the evolution and developmental origins of the vertebrate EOMs, we explored the development of the head mesoderm and EOMs of the lamprey in detail. We found that the disposition of lamprey EOM primordia differed from that in gnathostomes, even during the earliest period of development. We also found that three components of the paraxial head mesoderm could be distinguished genetically (premandibular mesoderm: Gsc+/TbxA-; mandibular mesoderm: Gsc-/TbxA-; hyoid mesoderm: Gsc-/TbxA+), indicating that the genetic mechanisms of EOMs are conserved in all vertebrates. We conclude that the tripartite developmental origin of the EOMs is likely to have been possessed by the latest common ancestor of the vertebrates. This ancestor's EOM developmental pattern was also suggested to have resembled more that of the lamprey, and the gnathostome EOMs' disposition is likely to have been established by a secondary modification that took place in the common ancestor of crown gnathostomes.

High amyloid-ß deposition related to depressive symptoms in older individuals with normal cognition: a pilot study.

OBJECTIVE: Previous studies have reported depressive symptoms in the preclinical stages of Alzheimer's disease (AD). The objective of this study was to determine whether depressive symptoms are associated with cortical amyloid burden. In order to do this, we measured cortical amyloid via (11) C-labeled Pittsburgh Compound B ([(11) C]PIB) uptake using positron emission tomography (PET) in cognitively normal subjects. METHODS: We performed [(11) C]PIB-PET in 29 cognitively normal, older participants. Depressive symptoms were assessed using the 15-item Geriatric Depression Scale (GDS). Aß deposition was quantified by binding potential (BPND ), and the association between cortical mean BPND values and GDS scores was evaluated. Analysis of parametric BPND images was performed to examine the relationship between regional BPND and GDS scores. RESULTS: We found a positive correlation between depressive symptoms and mean cortical PIB-BPND in groups of subjects with middle to high PIB-BPND . There was little change in GDS-depression score between subjects with low and middle PIB-BPND levels, while an increase in GDS was shown in the high PIB-BPND group. The main BPND increase was localized to the precuneus/posterior cingulate cortex (PCu/PCC) in subjects with high PIB-BPND , and we found a significant positive relationship between PIB-BPND in this area and depressive symptoms. CONCLUSIONS: Emotional dysregulation because of Aß neuropathology in the PCu/PCC may relate to depressive symptoms. More specifically, we found that older, cognitively normal patients with depressive episodes were more likely to have underlying AD pathology. Thus, depressive symptoms may increase the predictive ability of the identification of future AD cases. Copyright © 2016 John Wiley & Sons, Ltd.

A structural model of age, grey matter volumes, education, and personality traits.

BACKGROUND: When the relationship between ageing and changes in personality traits is considered, it is important to know how they are influenced by biological and environmental factors. The present study examined the relationships between various factors associated with the effect of ageing on personality traits, including structural changes of the brain and environmental factors such as education. METHODS: We recruited 41 healthy subjects. We administered the NEO Five-Factor Inventory to assess personality factors. Magnetic resonance imaging was performed, and regional grey matter (GM) volumes were obtained. We identified associations in the correlation analysis of age, cerebral GM volume, years of education, and the personality trait of openness. Path analysis was used to estimate the relationships among these factors. RESULTS: The path analysis model of age, GM volume, years of education, and the personality trait of openness revealed that age has an indirect negative association with openness through GM volume and years of education. Ageing was related to a decrease in GM volume, which was in turn related to a decrease in the openness score. Older subjects generally had fewer years of education, which was related to a lower openness score. CONCLUSIONS: Maintaining openness against the effects of ageing is desirable, and our results imply that interventions against age-related cerebral atrophy and the promotion of opportunities for higher education may contribute to the development and stability of a healthy personality during the adult life course.

Only extra-high dose of ketamine affects l-glutamate-induced intracellular Ca(2+) elevation and neurotoxicity.

The neurotoxic effects of anesthetics on the developing brain are a concern. Although most of the anesthetics are GABAA agonists or NMDA antagonists, the differences in these effects on prospective glutamate-neurotoxicity in the brain is not fully understood. We examined the degree of L-glutamate-induced intracellular calcium ([Ca(2+)]i) elevation and neurotoxicity in neurons exposed to anesthetics. Primary cortical neurons from E17 rats were preincubated with 1-100 µM of ketamine or thiopental sodium (TPS) for the first 72 h of culturing. Two weeks later, the neurons were exposed to L-glutamate. The extent of glutamate toxicity was evaluated using Ca(2+)-imaging and morphological experiments. Preincubation with 100 µM ketamine but not with other concentrations of ketamine and TPS for the first 72 h in culture significantly enhanced L-glutamate-induced [Ca(2+)]i elevation 2 weeks later. Morphology experiments showed that vulnerability to L-glutamate-mediated neurotoxicity was only altered in neurons preincubated with 100 µM ketamine but not with TPS. Although preincubation with high concentration of ketamine showed enhancement of L-glutamate-induced [Ca(2+)]i elevation 2 weeks later, long-term exposure to TPS or ketamine at clinical doses during developmental periods may not result in a dose-related potentiation of exogenous glutamate-induced neurotoxicity, once the intravenous anesthetics are discontinued.

Resting-state synchrony between the retrosplenial cortex and anterior medial cortical structures relates to memory complaints in subjective cognitive impairment.

Subjective cognitive impairment (SCI) is a clinical state characterized by subjective cognitive deficits without cognitive impairment. To test the hypothesis that this state might involve dysfunction of self-referential processing mediated by cortical midline structures, we investigated abnormalities of functional connectivity in these structures in individuals with SCI using resting-state functional magnetic resonance imaging. We performed functional connectivity analysis for 23 individuals with SCI and 30 individuals without SCI. To reveal the pathophysiological basis of the functional connectivity change, we performed magnetic resonance-diffusion tensor imaging. Positron emission tomography-amyloid imaging was conducted in 13 SCI and 15 nonSCI subjects. Individuals with SCI showed reduced functional connectivity in cortical midline structures. Reduction in white matter connections was related to reduced functional connectivity, but we found no amyloid deposition in individuals with SCI. The results do not necessarily contradict the possibility that SCI indicates initial cognitive decrements, but imply that reduced functional connectivity in cortical midline structures contributes to overestimation of the experience of forgetfulness.

Delayed atrophy in posterior cingulate cortex and apathy after stroke.

OBJECTIVE: A few studies have been performed on chronic structural changes after stroke. The primary purpose of the present study was to investigate regional cortical volume changes after the onset of stroke and to examine how the cortical volume changes affected neuropsychiatric symptoms. METHODS: Participants were 20 stroke patients and 14 control subjects. T1-MRI was performed twice, once at the subacute stage and again 6 months later, and whole brain voxel-based morphometric (VBM) analysis was used to detect significant cortical gray matter volume changes in patients. We also assessed the correlation between changes in cortical volumes and changes in neuropsychiatric symptoms during the 6 months following a stroke. RESULTS: In the present study, we found significant volume reductions in the anterior part of the posterior cingulate cortex (PCC) over the 6 months following a stroke by exploratory VBM analysis. We also found that the amount of volume change was significantly correlated with the change in apathy-scale scores during the 6 months poststroke. CONCLUSIONS: The present study suggests that delayed atrophic change is evident in the PCC 6 months after a stroke. There was greater apathetic change in the stroke patients with the larger volume reductions. The delayed atrophy of the PCC may reflect degeneration secondary to neuronal loss due to stroke. Such degeneration might have impaired control of goal-directed behavior, leading to the observed increase in apathy.

Low amyloid-ß deposition correlates with high education in cognitively normal older adults: a pilot study.

OBJECTIVE: Several epidemiological studies have found a lower incidence of Alzheimer's disease in highly educated populations, but the protective mechanism of education against the disease is still unclear. Our objective was to investigate the association between education and (11) C-labeled Pittsburgh Compound B (PIB) uptake with positron emission tomography in participants with normal cognitive ability. METHODS: We performed (11) C-labeled PIB positron emission tomography and neuropsychological testing in 30 cognitively normal older participants. Of the participants, 16 had a period of education less than 12 years (low-education group) and 14 had more than 13 years (high-education group). Amyloid-ß deposition was quantified by binding potential (BPND ) in several brain regions and was compared between the groups with different education levels. RESULTS: We found significantly higher cortical PIB-BPND in the cognitively normal participants with low education compared with the ones with high education. None of the brain regions in low-education group showed significantly lower BPND values. This finding was not affected by the inclusion of possible confounding variables such as age, sex, and general intelligence. Our findings indicated a reduced amyloid pathology in highly educated, cognitively normal, participants. CONCLUSIONS: Our findings lead to the proposal that early-life education has a negative association with Alzheimer's disease pathology. This proposal is not in opposition to the brain reserve hypothesis. People with more education might be prone to a greater inhibitory effect against amyloid-ß deposition before the preclinical stage. At the same time, they have a greater reserve capacity, and greater pathological changes are required for dementia to manifest.

Gray and white matter changes in subjective cognitive impairment, amnestic mild cognitive impairment and Alzheimer's disease: a voxel-based analysis study.

Subjective cognitive impairment may be a very early at-risk period of the continuum of dementia. However, it is difficult to discriminate at-risk states from normal aging. Thus, detection of the early pathological changes in the subjective cognitive impairment period is needed. To elucidate these changes, we employed diffusion tensor imaging and volumetry analysis, and compared subjective cognitive impairment with normal, mild cognitive impairment and Alzheimer's disease. The subjects in this study were 39 Alzheimer's disease, 43 mild cognitive impairment, 28 subjective cognitive impairment and 41 normal controls. There were no statistically significant differences between the normal control and subjective cognitive impairment groups in all measures. Alzheimer's disease and mild cognitive impairment had the same extent of brain atrophy and diffusion changes. These results are consistent with the hypothetical model of the dynamic biomarkers of Alzheimer's disease.

Increased binding of 5-HT1A receptors in a dissociative amnesic patient after the recovery process.

Dissociative amnesia is characterized by an inability to retrieve information already saved in memories. 5-HT has some role in neural regulatory control and may be related to the recovery from dissociative amnesia. To examine the role of 5-HT1A receptors in the recovery from dissociative amnesia, we performed two positron emission tomography (PET) scans on a 30-year-old patient of dissociative amnesia using [(11)C]WAY-100635, the first at amnesic state, and the second at the time he had recovered. Exploratory voxel-based analysis (VBA) was performed using SPM software. 5-HT1A BPND images were compared between the patient at amnesic and recovery states and healthy subjects (14 males, mean age 29.8 ± 6.45) with Jack-knife analysis. 5-HT1A receptor bindings of the patient at the recovery state were significantly higher than those of healthy subjects in the right superior and middle frontal cortex, left inferior frontal and orbitofrontal cortex and bilateral inferior temporal cortex. The increase in BPND values of recovery state was beyond 10% of those of amnesia state in these regions except in the right superior frontal cortex. We considered that neural regulatory control by the increase of 5-HT1A receptors in cortical regions played a role in the recovery from dissociative amnesia.

Microstructural abnormalities in white matter and their effect on depressive symptoms after stroke.

The aim of the study was to investigate the existence of microstructural abnormalities in the white matter of the brain in stroke patients, as well as the relationship between these microstructural abnormalities and changes in depressive symptoms over 6 months. Participants were 29 acute ischemic stroke patients and 37 healthy control subjects. Depressive symptoms were assessed in all subjects using the Hamilton Rating Scale for Depression and the Zung Self-rating Depression Scale. Whole brain voxel-based analysis was used to compare diffusion tensor imaging measures of Fractional Anisotropy (FA) between the groups. Six-month follow-up examinations were conducted. Patients showed significantly lower white matter FA values in the left and right anterior limbs of the internal capsule, and 6 months after the stroke they showed significantly increased FA values in these regions. We found a significant negative correlation between the increased ratio of the FA values and the change in depression scale scores at 6-month follow-up. Regional white matter damage may reflect abnormalities in neuroanatomical pathways related to the pathophysiology of depression.