Impaired motor control due to proprioceptive sensory loss in a patient with cerebral infarction localized to the postcentral gyrus.

OBJECTIVE: Most rehabilitative interventions following stroke emphasize the improvement of motor deficits but rarely address sensory function and sensorimotor control. We report here a case of cerebral infarction localized to the postcentral gyrus that presented with severe impairment of motor control due to profound proprioceptive sensory loss. We attempted to demonstrate the mechanism for the motor impairment using functional magnetic resonance imaging (fMRI). CASE REPORT: A 70-year-old woman developed abrupt loss of motor control of the right hand, concomitant with the loss of proprioception of the hand. An fMRI was conducted 12 days after stroke onset. Movement of the unaffected hand activated the normal sensorimotor network in the brain, including the contralateral primary sensorimotor cortex, supplementary motor areas, and ipsilateral cerebellum. However, movement of the affected hand activated only the contralateral primary motor cortex and activation of the cerebral sensorimotor network was severely depressed. Diffusion tensor tractography revealed that the corticospinal tracts were intact. Intensive rehabilitation and the use of visual support enabled the patient to live an independent life. CONCLUSION: Loss of motor control may occur even with a normal corticospinal tract when proprioception is severely impaired by dysfunction of the sensorimotor network in the brain.

Neural basis of impaired cognitive flexibility in patients with anorexia nervosa.

BACKGROUND: Impaired cognitive flexibility in anorexia nervosa (AN) causes clinical problems and makes the disease hard to treat, but its neural basis has yet to be fully elucidated. The purpose of this study was to evaluate the brain activity of individuals with AN while performing a task requiring cognitive flexibility on the Wisconsin Card Sorting Test (WCST), which is one of the most frequently used neurocognitive measures of cognitive flexibility and problem-solving ability. METHODS: Participants were 15 female AN patients and 15 age- and intelligence quotient-matched healthy control women. Participants completed the WCST while their brain activity was measured by functional magnetic resonance imaging during the task. Brain activation in response to set shifting error feedback and the correlation between such brain activity and set shifting performance were analyzed. RESULTS: The correct rate on the WCST was significantly poorer for AN patients than for controls. Patients showed poorer activity in the right ventrolateral prefrontal cortex and bilateral parahippocampal cortex on set shifting than controls. Controls showed a positive correlation between correct rate and ventrolateral prefrontal activity in response to set shifting whereas patients did not. CONCLUSION: These findings suggest dysfunction of the ventrolateral prefrontal cortex and parahippocampal cortex as a cause of impaired cognitive flexibility in AN patients.

Altered cognitive function of prefrontal cortex during error feedback in patients with irritable bowel syndrome, based on FMRI and dynamic causal modeling.

BACKGROUND & AIMS: Patients with irritable bowel syndrome (IBS) have increased activity in the insula and reduced activation of the dorsolateral prefrontal cortex (DLPFC) in response to visceral stimulation. We investigated whether they have latent impairments in cognitive flexibility because of dysfunction in the DLPFC and insula and altered connectivity between brain regions. METHODS: We analyzed data from 30 individuals with IBS (15 men; age, 21.7 ± 3.0 y) diagnosed based on Rome III criteria, along with 30 individuals matched for age, sex, and education level (controls). Event-related functional magnetic resonance imaging of the brain was performed to evaluate cognitive flexibility and was assessed by the Wisconsin Card Sorting Test, in which subjects are allowed to change choice criteria, defined as set-shifting in response to error feedback. Brain images were analyzed with statistical parametric mapping 5 and 8 software and dynamic causal modeling. RESULTS: Subjects with IBS had significantly more Nelson perseverative errors (P < .05) and set-maintenance difficulties (P < .05) than controls. They also showed significantly decreased activity of the right DLPFC (Brodmann's area 9; P < .001) and right hippocampus (P < .001), and significantly increased activity of the left posterior insula (P < .001) at error feedback during set-shifting. Dynamic causal modeling analysis during set-shifting revealed significantly less connectivity from the DLPFC to pre-supplementary motor area in subjects with IBS, compared with controls (P = .012). CONCLUSIONS: Individuals with IBS have latent impairments in cognitive flexibility as a result of altered activity of the DLPFC, insula, and hippocampus, and impaired connectivity between the DLPFC and pre-supplementary motor area.

A prominent elevation of glial fibrillary acidic protein in the cerebrospinal fluid during relapse in neuromyelitis optica.

Neuromyelitis optica (NMO) is a neurologic disease characterized by severe optic neuritis, longitudinally extended, transverse myelitis and serum aquaporin-4 (AQP4) antibody. Our recent neuropathological study revealed the extensive loss of AQP4 and glial fibrillary acidic protein (GFAP), an astrocyte-specific protein, in NMO lesions, but not in MS lesions, suggesting that severe astrocytic damage or dysfunction may be related to the pathogenesis of NMO. Here we report a patient of NMO, in which the cerebrospinal fluid (CSF) levels of GFAP were measured both during relapse of myelitis and after high-dose intravenous methylprednisolone (HIMP). The patient was a 34-year old woman with two previous episodes of optic neuritis. She developed myelitis longitudinally extending from C3 to T12 with contrast enhancement, and was AQP4 antibody-positive. In the acute phase, the GFAP level in the cerebrospinal fluid (CSF) was prominently elevated (18,966.7 ng/ml) as compared with controls (0.6 +/- 0.33 ng/ml). However, following HIMP, the clinical and MRI findings improved, and the CSF-GFAP level was near-normal (2.1 ng/ml). The CSF of myelin basic protein was also elevated in relapse (1,016.0 pg/ml), and became lower but still remained high (158.7 pg/ml) after HIMP compared with controls (3.36 +/- 3.83 pg/ml). The prominent elevation of the CSF-GFAP level in relapse of NMO, followed by its sharp decline after therapy, suggests severe astrocytic damage with a temporal profile distinct from that of the demyelinating process in NMO. CSF-GFAP may be useful as a biomarker of NMO.

Near-infrared spectroscopic topography as a tool to monitor motor reorganization after hemiparetic stroke: a comparison with functional MRI.

BACKGROUND AND PURPOSE: Motor functional recovery from stroke can occur, but the mechanisms underlying this restorative process remain to be elucidated. We used near-infrared spectroscopic (NIRS) topography in comparison with functional MRI (fMRI) to evaluate the compensatory motor activation of cortical regions in patients who recovered from hemiparesis after cortical cerebral infarction. METHODS: We examined 6 right-handed patients who suffered cerebral infarction of the middle cerebral artery territory with minimal or mild residual contralateral hemiparesis (4 men and 2 women, 59 to 79 years old, all had left hemiparesis). Both fMRI and NIRS were studied during a hand movement task at chronic stages. Five right-handed, normal subjects (3 men and 2 women, 44 to 81 years old) served as controls. RESULTS: fMRI and NIRS detected very similar cerebral cortical activation, although NIRS detected only superficial activation. The spatial resolution of NIRS was less than that of fMRI, but NIRS provided a dynamic profile of activation. Normal subjects activated predominantly the contralateral primary sensorimotor cortex and supplementary motor areas during each hand movement. All the stroke patients exhibited the normal activation pattern during normal hand movement. On affected hand movement, the stroke patients showed extended activation not only in the contralateral motor cortex but also in the ipsilateral motor cortex (primary motor cortex and supplementary motor areas). CONCLUSIONS: Both fMRI and NIRS studies provided evidence for the contribution of ipsilateral motor cortical compensation or reorganization to the recovery from poststroke hemiparesis. The result demonstrated that NIRS was a unique tool to monitor poststroke alterations in cortical motor functions.

Silent cerebral microbleeds on T2*-weighted MRI: correlation with stroke subtype, stroke recurrence, and leukoaraiosis.

BACKGROUND AND PURPOSE: Gradient-echo T2*-weighted MRI is uniquely sensitive to detect silent, old hemosiderin deposits, but the clinical significance of such "microbleeds" remains to be determined. Therefore, we investigated the incidence and the number of microbleeds among different stroke subtypes and the correlation with stroke recurrence and the severity of leukoaraiosis. METHODS: This study consisted of 213 patients (73.5+/-9.1 years old, 104 men and 109 women), who were classified according to stroke subtypes into atherothrombotic infarction (24 patients), cardioembolic infarction (23 patients), lacunar infarction (66 patients), intracerebral hemorrhage (35 patients), and control (65 patients) groups. Gradient-echo T2*-weighted MRI was performed with a 1.5 T system, and asymptomatic microbleeds were located and counted. RESULTS: The incidence and the number of microbleeds were significantly greater in patients with intracerebral hemorrhage (71.4% and 9.1+/-13.8, respectively) and lacunar infarction (62.1% and 7.4+/-16.1) compared with patients with cardioembolic infarction (30.4% and 2.5+/-5.6), atherothrombotic infarction (20.8% and 0.63+/-1.53), and controls (7.7% and 0.09+/-0.34). There was a correlation between the number of microbleeds and the severity of periventricular hyperintensity (r=0.626, P<0.0001). There was also a correlation between the number of microbleeds and the number of intracerebral hemorrhages (r=0.689, P<0.0001) or lacunar infarctions (r=0.514, P<0.0001). The locations of microbleeds were subcortical white matter (31.8%), thalamus (24.8%), basal ganglia (19.8%), brain stem (12.0%), and cerebellum (11.7%). CONCLUSIONS: The findings suggest that microbleeds on T2*-weighted MRI are an indicator of advanced small artery disease of the brain with an increased risk for bleeding. This result should be taken into consideration when treating patients with stroke, and further studies are required.

Orderly activations of human cortical areas during path-planning task.

The functional anatomy of planning was investigated using a path-planning task, which required subjects to find a path to a goal that avoided obstacles and then move a cursor along the path to the goal by manipulating four switches. We analyzed event-related activation in response to four consecutive events during the path-planning task using fMRI. We classified activated cortical regions into four groups based on when each cortical region showed the most significant activation in response to behavioral events during the path-planning task. Our data suggested that each prefrontal and motor cortical area was involved in a different phase of path planning.