Decreased amygdala-sensorimotor connectivity mediates the association between prenatal stress and broad autism phenotype in young adults: Project Ice Storm.

Studies show that prenatal maternal stress (PNMS) is related to risk for child autism, and to atypical amygdala functional connectivity in the autistic child. Yet, it remains unclear whether amygdala functional connectivity mediates the association between PNMS and autistic traits, particularly in young adult offspring. We recruited women who were pregnant during, or within 3 months of, the 1998 Quebec ice storm crisis, and assessed three aspects of PNMS: objective hardship (events experienced during the ice storm), subjective distress (post-traumatic stress symptoms experienced as a result of the ice storm) and cognitive appraisal. At age 19, 32 young adults (21 females) self-reported their autistic-like traits (i.e., aloof personality, pragmatic language impairment and rigid personality), and underwent structural MRI and resting-state functional MRI scans. Seed-to-voxel analyses were conducted to map the amygdala functional connectivity network. Mediation analyses were implemented with bootstrapping of 20,000 resamplings. We found that greater maternal objective hardship was associated with weaker functional connectivity between the left amygdala and the right postcentral gyrus, which was then associated with more pragmatic language impairment. Greater maternal subjective distress was associated with weaker functional connectivity between the right amygdala and the left precentral gyrus, which was then associated with more aloof personality. Our results demonstrate that the long-lasting effect of PNMS on offspring autistic-like traits may be mediated by decreased amygdala-sensorimotor circuits. The differences between amygdala-sensory and amygdala-motor pathways mediating different aspects of PNMS on different autism phenotypes need to be studied further.

Beyond Broca: neural architecture and evolution of a dual motor speech coordination system.

Classical neural architecture models of speech production propose a single system centred on Broca's area coordinating all the vocal articulators from lips to larynx. Modern evidence has challenged both the idea that Broca's area is involved in motor speech coordination and that there is only one coordination network. Drawing on a wide range of evidence, here we propose a dual speech coordination model in which laryngeal control of pitch-related aspects of prosody and song are coordinated by a hierarchically organized dorsolateral system while supralaryngeal articulation at the phonetic/syllabic level is coordinated by a more ventral system posterior to Broca's area. We argue further that these two speech production subsystems have distinguishable evolutionary histories and discuss the implications for models of language evolution.

Abnormal brain regional activity in acute thyrotoxic myopathy assessed by resting-state functional MRI.

BACKGROUND: The neurophysiological mechanisms underlying manifestations of bulbar paralysis in acute thyrotoxic myopathy (ATM) and the afflicted brain areas are unclear. PURPOSE: We used resting-state functional magnetic resonance imaging (rs-fMRI) to evaluate the regional brain activities in patients with ATM. MATERIAL AND METHODS: In total, 16 patients with ATM, 16 patients with hyperthyroidism without ATM, and 16 healthy controls underwent functional MRI scans. By calculating the fractional amplitude of low-frequency fluctuation (fALFF), regional homogeneity (ReHo), and functional connectivity (FC), we assessed variations in resting-state cerebral activity. The correlation between the resting-state functional indexes and clinical assessments was also explored. RESULTS: Compared to the hyperthyroid patients, patients with ATM had stronger ReHo in the left precentral gyrus, reduced ReHo in the left orbitofrontal gyrus (OFG), and decreased FC in the left precentral gyri, left superior frontal gyrus (SFG), and left middle frontal gyrus (MFG). Patients with ATM showed reduced fALFF and ReHo in the right SFG and decreased ReHo in the bilateral supplementary motor area (SMA). A significantly decreased FC in the left SFG and left MFG, right precentral gyrus, and the orbital part of the right interior frontal gyrus was observed in patients with ATM compared to healthy controls. Additionally, fALFF and ReHo values were positively correlated with serum thyroid-related hormones and antibodies. CONCLUSION: The findings of rs-fMRI demonstrate that particular brain regions' functional activity was aberrant in individuals with ATM, especially in SFG area. This finding may help with better understanding of underlying pathophysiology of patients with ATM.

Targeting Lower Limb, Upper Limb, and Face Representation in the Primary Motor Cortex for the Practice of Neuronavigated Transcranial Magnetic Stimulation.

OBJECTIVE: The primary motor cortex (M1) is a usual target for therapeutic application of repetitive transcranial magnetic stimulation (rTMS), especially the region of hand motor representation. However, other M1 regions can be considered as potential rTMS targets, such as the region of lower limb or face representation. In this study, we assessed the localization of all these regions on magnetic resonance imaging (MRI) with the aim of defining three standardized M1 targets for the practice of neuronavigated rTMS. MATERIALS AND METHODS: A pointing task of these targets was performed by three rTMS experts on 44 healthy brain MRI data to assess interrater reliability (including the calculation of intraclass correlation coefficients [ICCs] and coefficients of variation [CoVs] and the construction of Bland-Altman plots). In addition, two "standard" brain MRI data were randomly interspersed with the other MRI data to assess intrarater reliability. A barycenter was calculated for each target (with x-y-z coordinates provided in normalized brain coordinate systems), in addition to the geodesic distance between the scalp projection of the barycenters of these different targets. RESULTS: Intrarater and interrater agreement was good, according to ICCs, CoVs, or Bland-Altman plots, although interrater variability was greater for anteroposterior (y) and craniocaudal (z) coordinates, especially for the face target. The scalp projection of the barycenters between the different cortical targets ranged from 32.4 to 35.5 mm for either the lower-limb-to-upper-limb target distance or the upper-limb-to-face target distance. CONCLUSIONS: This work clearly delineates three different targets for the application of motor cortex rTMS that correspond to lower limb, upper limb, and face motor representations. These three targets are sufficiently spaced to consider that their stimulation can act on distinct neural networks.

A Narrative Review of Stroke of Cortical Hand Knob Area.

The cortical hand knob region of the brain is a knob-like segment of the precentral gyrus, projecting into the middle genu of the central sulcus. This anatomic landmark is responsible for intricate control of hand motor movements and has often been implicated in motor weakness following stroke. In some instances, damage to this area has been mistaken for peripheral causes of hand weakness. Our article aims to consolidate clinically relevant information on the cortical hand knob area in a comprehensive review to guide clinicians regarding diagnosis and treatment strategies. We conducted a systematic search within the Medline/PubMed database for reports of strokes in the cortical hand knob region. All studies were published electronically up until December 2023. The search was conducted using the keyword "hand knob". A total of 24 reports containing 150 patients were found. The mean and median ages were 65 and 67 years, respectively. Sixty-two percent of the individuals were male. According to the TOAST criteria for the classification of the stroke, 59 individuals had a stroke due to large-artery atherosclerosis, 8 had small-vessel occlusion, 20 had cardioembolism, 25 were determined, and 38 were undetermined. The most common etiologies for stroke in the hand knob area can be attributed to large vessel occlusions, small vessel occlusions, or cardioembolism. Presentations following damage to this area can mimic ulnar, median, or radial neuropathy as well. Our comprehensive review serves as a resource for recognizing and managing stroke in the cortical hand knob area.

Speech apraxia and oral apraxia: association or dissociation? A multivariate lesion-symptom mapping study in acute stroke patients.

The anatomical relationship between speech apraxia (SA) and oral apraxia (OA) is still unclear. To shed light on this matter we studied 137 patients with acute ischaemic left-hemisphere stroke and performed support vector regression-based, multivariate lesion-symptom mapping. Thirty-three patients presented with either SA or OA. These two symptoms mostly co-occurred (n = 28), except for few patients with isolated SA (n = 2) or OA (n = 3). All patient with either SA or OA presented with aphasia (p < 0.001) and these symptoms were highly associated with apraxia (p < 0.001). Co-occurring SA and OA were predominantly associated with insular lesions, while the insula was completely spared in the five patients with isolated SA or OA. Isolated SA occurred in case of frontal lesions (prefrontal gyrus and superior longitudinal fasciculus), while isolated OA occurred in case of either temporoparietal or striatocapsular lesions. Our study supports the notion of a predominant, but not exclusive, role of the insula in verbal and non-verbal oral praxis, and indicates that frontal regions may contribute exclusively to verbal oral praxis, while temporoparietal and striatocapsular regions contribute to non-verbal oral praxis. However, since tests for SA and OA so far intrinsically also investigate aphasia and apraxia, refined tests are warranted.

Inflammation is correlated with abnormal functional connectivity in unmedicated bipolar depression: an independent component analysis study of resting-state fMRI.

BACKGROUND: Inflammation might play a role in bipolar disorder (BD), but it remains unclear the relationship between inflammation and brain structural and functional abnormalities in patients with BD. In this study, we focused on the alterations of functional connectivity (FC), peripheral pro-inflammatory cytokines and their correlations to investigate the role of inflammation in FC in BD depression. METHODS: In this study, 42 unmedicated patients with BD II depression and 62 healthy controls (HCs) were enrolled. Resting-state-functional magnetic resonance imaging was performed in all participants and independent component analysis was used. Serum levels of Interleukin-6 (IL-6) and Interleukin-8 (IL-8) were measured in all participants. Correlation between FC values and IL-6 and IL-8 levels in BD was calculated. RESULTS: Compared with the HCs, BD II patients showed decreased FC in the left orbitofrontal cortex (OFC) implicating the limbic network and the right precentral gyrus implicating the somatomotor network. BD II showed increased IL-6 (p = 0.039), IL-8 (p = 0.002) levels. Moreover, abnormal FC in the right precentral gyrus were inversely correlated with the IL-8 (r = -0.458, p = 0.004) levels in BD II. No significant correlation was found between FC in the left OFC and cytokines levels. CONCLUSIONS: Our findings that serum IL-8 levels are associated with impaired FC in the right precentral gyrus in BD II patients suggest that inflammation might play a crucial role in brain functional abnormalities in BD.

Structural and functional underpinnings of precentral abnormalities in amyotrophic lateral sclerosis.

BACKGROUND AND PURPOSE: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by the loss of both upper and lower motor neurons. Studies using various magnetic resonance imaging (MRI) analytical approaches have consistently identified significant precentral abnormalities in ALS, whereas their structural and functional underpinnings remain poorly understood. METHODS: Using cortical thickness, fractional anisotropy (FA), and effective connectivity, we performed a multimodal MRI study to examine the structural and functional alterations associated with precentral abnormalities in patients with ALS (n = 60) compared with healthy controls (n = 60). RESULTS: Cortical thickness analysis revealed significant cortical thinning in the right precentral gyrus (PCG), superior frontal gyrus, and superior temporal gyrus in patients with ALS. Tractwise white matter microstructure analyses revealed decreased FA in the tracts connected to the PCG cluster in patients with ALS involving the right corticospinal tract and the middle posterior body of the corpus callosum. Additionally, the cortical thickness of the PCG cluster was found to be positively correlated with FA of the tracts connected to the PCG cluster, suggesting that these two structural features are tightly coupled. Using spectral dynamic causal modelling, effective connectivity analysis among the three regions with cortical thinning revealed decreased self-inhibitory influence in the PCG cluster in patients with ALS, which might be an endophenotypic manifestation of an imbalance in inhibitory and excitatory neurotransmitters in this region. CONCLUSIONS: The present data shed new light on the structural and functional underpinnings of precentral abnormalities in ALS.

Amyotrophic lateral sclerosis with speech apraxia, predominant upper motor neuron signs, and prominent iron accumulation in the frontal operculum and precentral gyrus.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease; transactivation response DNA-binding protein of 43 kDa (TDP-43) and iron accumulation are supposed to play a crucial role in the pathomechanism of the disease. Here, we report an unusual case of a patient with ALS who presented with speech apraxia as an initial symptom and upper motor neuron deficiencies. In the early clinical stages, single-photon emission computed tomography visualized focal hypoperfusion of the right frontal operculum, and magnetic resonance imaging identified a hypointense area along the frontal lobe on T2-weighted images. Neuropathological examination revealed that neuronophagia of Betz cells, gliosis, appearance of phosphorylated TDP-43 (p-TDP-43)-positive glial and neuronal inclusions, and prominent iron accumulation were frequently visible in the precentral gyrus. TDP-43 pathology and focal iron accumulation were also visible in the frontal operculum, but only a mild neuronal loss and a few p-TDP-43-positive neuronal and glial inclusions were found in the hypoglossal nucleus of the medulla oblongata and anterior horn of the spinal cord. Immunoblot analysis revealed an atypical band pattern for ALS. In our case, abnormal TDP-43 and iron accumulation might possibly have caused neurodegeneration of the frontal operculum, in tandem or independently; it might then have spread into the primary motor area. Our results suggest a causative association between TDP-43 and iron accumulation in the pathomechanisms of ALS presenting with upper motor neuron signs.

Structural brain abnormalities in the common epilepsies assessed in a worldwide ENIGMA study.

Progressive functional decline in the epilepsies is largely unexplained. We formed the ENIGMA-Epilepsy consortium to understand factors that influence brain measures in epilepsy, pooling data from 24 research centres in 14 countries across Europe, North and South America, Asia, and Australia. Structural brain measures were extracted from MRI brain scans across 2149 individuals with epilepsy, divided into four epilepsy subgroups including idiopathic generalized epilepsies (n =367), mesial temporal lobe epilepsies with hippocampal sclerosis (MTLE; left, n = 415; right, n = 339), and all other epilepsies in aggregate (n = 1026), and compared to 1727 matched healthy controls. We ranked brain structures in order of greatest differences between patients and controls, by meta-analysing effect sizes across 16 subcortical and 68 cortical brain regions. We also tested effects of duration of disease, age at onset, and age-by-diagnosis interactions on structural measures. We observed widespread patterns of altered subcortical volume and reduced cortical grey matter thickness. Compared to controls, all epilepsy groups showed lower volume in the right thalamus (Cohen's d = -0.24 to -0.73; P < 1.49 × 10-4), and lower thickness in the precentral gyri bilaterally (d = -0.34 to -0.52; P < 4.31 × 10-6). Both MTLE subgroups showed profound volume reduction in the ipsilateral hippocampus (d = -1.73 to -1.91, P < 1.4 × 10-19), and lower thickness in extrahippocampal cortical regions, including the precentral and paracentral gyri, compared to controls (d = -0.36 to -0.52; P < 1.49 × 10-4). Thickness differences of the ipsilateral temporopolar, parahippocampal, entorhinal, and fusiform gyri, contralateral pars triangularis, and bilateral precuneus, superior frontal and caudal middle frontal gyri were observed in left, but not right, MTLE (d = -0.29 to -0.54; P < 1.49 × 10-4). Contrastingly, thickness differences of the ipsilateral pars opercularis, and contralateral transverse temporal gyrus, were observed in right, but not left, MTLE (d = -0.27 to -0.51; P < 1.49 × 10-4). Lower subcortical volume and cortical thickness associated with a longer duration of epilepsy in the all-epilepsies, all-other-epilepsies, and right MTLE groups (beta, b < -0.0018; P < 1.49 × 10-4). In the largest neuroimaging study of epilepsy to date, we provide information on the common epilepsies that could not be realistically acquired in any other way. Our study provides a robust ranking of brain measures that can be further targeted for study in genetic and neuropathological studies. This worldwide initiative identifies patterns of shared grey matter reduction across epilepsy syndromes, and distinctive abnormalities between epilepsy syndromes, which inform our understanding of epilepsy as a network disorder, and indicate that certain epilepsy syndromes involve more widespread structural compromise than previously assumed.

Autopsied case with MERRF/MELAS overlap syndrome accompanied by stroke-like episodes localized to the precentral gyrus.

We present an autopsied case with A8344G-mutated myoclonus epilepsy with ragged red fibers (MERRF)/mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) overlap syndrome accompanied by stroke-like episodes localized to the precentral gyrus. A 16-year-old Japanese woman suddenly experienced repetitive consciousness disturbances with increased serum lactate and creatine kinase levels. Magnetic resonance imaging showed abnormal intensity of bilateral precentral gyrus. She was clinically diagnosed as having a mitochondrial disorder and the A8344G mutation was detected in mitochondrial DNA. At 17 years of age, she died from congestive heart failure secondary to a third episode of lactic acidosis. Neuropatho-logically, multifocal laminar necrosis, which is responsible for stroke-like episodes in MELAS, was seen in the frontal cortex including the precentral gyrus, but there was no neuronal loss and gliosis in the basal ganglia, cerebellum, and brainstem, which were compatible with MERRF. Hypertrophy of the vascular smooth muscle and choroidal epithelium were seen, and were strongly visualized by an anti-mitochondrial antibody. Skeletal muscles showed uneven muscular diameters, increased central nuclei, and ragged red fibers (RRFs). Decreased cytochrome c oxidase (COX) activity and strongly succinate dehydrogenase (SDH)-reactive blood vessels were also noted. Stroke-like episodes in MERRF/MELAS overlap syndrome are thought to be rare in the frontal cortex including the precentral gyrus. Only two cases of MERRF/MELAS overlap syndrome with A8344G mutation, including this case, have shown stroke-like episodes in the frontal lobes. Other than the A8344G mutation and frontal lobe involvement, they had a high degree of similarity in terms of presence of RRFs, gastrointestinal dysfunction, and lack of typical MERRF neuropathology. In conclusion, this is an important case describing the clinical spectrum associated with A8344G-mutated MERRF/MELAS overlap syndrome.

The heterogeneity of the left dorsal premotor cortex evidenced by multimodal connectivity-based parcellation and functional characterization.

Despite the common conception of the dorsal premotor cortex (PMd) as a single brain region, its diverse connectivity profiles and behavioral heterogeneity argue for a differentiated organization of the PMd. A previous study revealed that the right PMd is characterized by a rostro-caudal and a ventro-dorsal distinction dividing it into five subregions: rostral, central, caudal, ventral and dorsal. The present study assessed whether a similar organization is present in the left hemisphere, by capitalizing on a multimodal data-driven approach combining connectivity-based parcellation (CBP) based on meta-analytic modeling, resting-state functional connectivity, and probabilistic diffusion tractography. The resulting PMd modules were then characterized based on multimodal functional connectivity and a quantitative analysis of associated behavioral functions. Analyzing the clusters consistent across all modalities revealed an organization of the left PMd that mirrored its right counterpart to a large degree. Again, caudal, central and rostral modules reflected a cognitive-motor gradient and a premotor eye-field was found in the ventral part of the left PMd. In addition, a distinct module linked to abstract cognitive functions was observed in the rostro-ventral left PMd across all CBP modalities, implying greater differentiation of higher cognitive functions for the left than the right PMd.

Region-specific atrophy of precentral gyrus in patients with amyotrophic lateral sclerosis.

PURPOSE: To assess the region-specific atrophy of precentral gyrus (PrCG) and its correlation to clinical function score in amyotrophic lateral sclerosis (ALS). MATERIALS AND METHODS: Twenty-eight patients with sporadic ALS and 28 healthy controls underwent high-resolution 3D T1-BRAVO magnetic resonance imaging at 3T. The bilateral PrCG segmentations were automatically obtained from a validated segmentation pipeline based on diffeomorphic multi-atlas likelihood fusion. Patients with ALS were further subclassified into early-stage (ALS-e, n = 22) and late-stage (ALS-l, n = 6) groups, with 12 months as a disease duration cutoff. Vertex-based shape analysis was performed to quantify the region-specific abnormalities of PrCG in ALS subgroups as compared to controls. In addition, we tested the statistical association between altered PrCG morphometry and clinical disability in ALS as evaluated by the revised ALS Functional Rating Scale (ALSFRS-r). RESULTS: Compared to controls, vertex-wise analysis showed that both ALS-e and ALS-l had significant atrophy of the dorsal-lateral part of PrCG (P < 0.05, uncorrected). Importantly, atrophy in ALS-e was not as widespread as that in ALS-l; while atrophy in ALS-e was mostly confined to the dorsal-lateral region (P < 0.05, uncorrected, surface areas exhibiting significant difference at a level of P = 0.05: left 613.88 mm2 , right 937.80 mm2 ), atrophy in ALS-l occurred at the dorsal-medial and ventral region as well (P < 0.05, uncorrected, surface areas exhibiting significant difference at a level of P = 0.05: left 1465.98 mm2 , right 1253.89 mm2 ). Partial correlation analysis showed that the significant surface area atrophy of PrCG in ALS, especially that of the dorsal-lateral portion, was found to link tightly with ALSFRS-r (P < 0.05, uncorrected, surface areas exhibiting significant correlation: left 723.08 mm2 , right 474.24 mm2 ). CONCLUSION: Our findings suggest that an altered PrCG morphometry, especially atrophy of the surface area in the dorsal-lateral portion, may be associated with the dysfunction that characterizes ALS. This study is an initial attempt to apply a validated statistical shape analysis pipeline to cortical gray matter structure like PrCG. LEVEL OF EVIDENCE: 1 Technical Efficacy Stage: 1 J. Magn. Reson. Imaging 2018;47:115-122.

An autopsy case of globular glial tauopathy presenting with clinical features of motor neuron disease with dementia and iron deposition in the motor cortex.

Globular glial tauopathy (GGT) is a 4-repeat (4R) tauopathy in which 4R tau accumulates to form globular glial inclusions (GGIs), predominantly in oligodendroglia. To date, little has been reported on iron deposits in patients with GGT. We report a case of GGT with iron deposits in a 78-year-old woman presenting with an 8-year history of slowly progressing limb weakness and cognitive decline. Susceptibility-weighted imaging revealed a low signal intensity in the right precentral gyrus, suggesting iron deposition. A clinical diagnosis of motor neuron disease with dementia was made 4 years after onset. At autopsy, gross pathological findings showed atrophy of the frontal and temporal lobes. A localized area of the precentral gyrus corresponding to the most severely affected limb showed the strongest atrophy, macroscopically, and displayed 4R tau-immunoreactive GGIs and microscopically many ferritin-immunoreactive neurons. We diagnosed this patient as having GGT. This is the first GGT case with iron deposition confirmed both radiologically and pathologically.

Cortical Hand Knob Stroke: Report of 25 Cases.

BACKGROUND: Although uncommon, cortical hand knob territory stroke is a well-defined stroke entity that mimics peripheral nerve damage. Atherosclerosis and hypertension are the most prevalent risk factors for the disease. Embolic origin, either artery-to-artery or cardioembolic, has been suggested as the most probable underlying mechanism. MATERIALS AND METHODS: Twenty-five patients with isolated hand palsy due to central origin were admitted to our department between 2006 and 2016. Cortical lesions were proven by either computed tomography or magnetic resonance imaging. RESULTS: The average age was 67 ± 12 years. Most of the cases were first-ever strokes (n = 23, 92%). Isolated infarct in the hand knob region was found in 18 of the 25 cases, whereas 7 had multiple acute infarctions. Supra-aortic atherosclerosis was found in 21 patients, 8 of them had 50% or greater ipsilateral stenosis of the internal carotid artery. Hypertension was the second most prevalent risk factor (n = 20, 80%). Quick improvement of symptoms was seen in almost every case (mean follow-up 17.5 months), 9 patients showed complete recovery, whereas 2 remained disabled and 1 died due to a malignant disease. Three patients suffered a recurrent stroke on follow-up. CONCLUSIONS: We conclude that distal arm paresis is a rare presentation of acute stroke with usually benign course.

A pilot study exploring the association of morphological changes with 5-HTTLPR polymorphism in OCD patients.

BACKGROUND: Clinical and pharmacological studies of obsessive-compulsive disorder (OCD) have suggested that the serotonergic systems are involved in the pathogenesis, while structural imaging studies have found some neuroanatomical abnormalities in OCD patients. In the etiopathogenesis of OCD, few studies have performed concurrent assessment of genetic and neuroanatomical variables. METHODS: We carried out a two-way ANOVA between a variable number of tandem repeat polymorphisms (5-HTTLPR) in the serotonin transporter gene and gray matter (GM) volumes in 40 OCD patients and 40 healthy controls (HCs). RESULTS: We found that relative to the HCs, the OCD patients showed significant decreased GM volume in the right hippocampus, and increased GM volume in the left precentral gyrus. 5-HTTLPR polymorphism in OCD patients had a statistical tendency of stronger effects on the right frontal pole than those in HCs. CONCLUSIONS: Our results showed that the neuroanatomical changes of specific GM regions could be endophenotypes of 5-HTTLPR polymorphism in OCD.

Is an absolute level of cortical beta suppression required for proper movement? Magnetoencephalographic evidence from healthy aging.

Previous research has connected a specific pattern of beta oscillatory activity to proper motor execution, but no study to date has directly examined how resting beta levels affect motor-related beta oscillatory activity in the motor cortex. Understanding this relationship is imperative to determining the basic mechanisms of motor control, as well as the impact of pathological beta oscillations on movement execution. In the current study, we used magnetoencephalography (MEG) and a complex movement paradigm to quantify resting beta activity and movement-related beta oscillations in the context of healthy aging. We chose healthy aging as a model because preliminary evidence suggests that beta activity is elevated in older adults, and thus by examining older and younger adults we were able to naturally vary resting beta levels. To this end, healthy younger and older participants were recorded during motor performance and at rest. Using beamforming, we imaged the peri-movement beta event-related desynchronization (ERD) and extracted virtual sensors from the peak voxels, which enabled absolute and relative beta power to be assessed. Interestingly, absolute beta power during the pre-movement baseline was much stronger in older relative to younger adults, and older adults also exhibited proportionally large beta desynchronization (ERD) responses during motor planning and execution compared to younger adults. Crucially, we found a significant relationship between spontaneous (resting) beta power and beta ERD magnitude in both primary motor cortices, above and beyond the effects of age. A similar link was found between beta ERD magnitude and movement duration. These findings suggest a direct linkage between beta reduction during movement and spontaneous activity in the motor cortex, such that as spontaneous beta power increases, a greater reduction in beta activity is required to execute movement. We propose that, on an individual level, the primary motor cortices have an absolute threshold of beta power that must be reached in order to move, and that an inability to suppress beta power to this threshold results in an increase in movement duration.

Zebra sign of precentral gyri in amyotrophic lateral sclerosis: A novel finding using phase difference enhanced (PADRE) imaging-initial results.

OBJECTIVE: We compared the precentral gyri (PG) on the PADRE of patients with amyotrophic lateral sclerosis (ALS) and healthy subjects (HSs) in order to determine whether it is possible to discriminate between ALS patients and HSs on an individual basis. METHODS: First, two radiologists reviewed the appearance of the normal PG and that of ALS patients on PADRE in a non-blinded manner, and deviations from the appearance of the normal PG were recorded. Next, based on the presence of PG abnormalities on PADRE, we performed an observer performance study using 16 ALS patients and 16 HSs. RESULTS: The radiologists were able to consensually define the PG as abnormal on PADRE when a low-signal-intensity layer was observed in the gray matter of the PG; a three- or four-layer organization (zebra sign) was characterized by the low-signal-intensity layer. The observer performance study demonstrated that the sensitivity, specificity, and accuracy of PG abnormalities on PADRE for discriminating ALS patients from HSs were 94 %, 94 %, and 94 %, respectively, for reviewers 1 and 2. CONCLUSIONS: It was possible to discriminate between ALS patients and HSs based on the presence of PG abnormalities on PADRE, which may reflect upper motor neuron impairment in ALS. KEY POINTS: • PADRE reveals low-signal-intensity layer in the PG of ALS • By PADRE findings on PG, we can discriminate ALS from HSs • PADRE may be a useful method for detecting UMN impairment in ALS.

Signal intensity of superficial white matter on phase difference enhanced imaging as a landmark of the perirolandic cortex.

Background The superficial white matter (SWM), which fills the space between the deep white matter and the cortex, has not been well characterized. Purpose To determine whether the assessment of the relative signal intensity (SI) of the SWM in the precentral and postcentral gyri on phase difference enhanced (PADRE) images contributes in establishing anatomical landmark. Material and Methods The study population consisted of 43 normal subjects (28 women, 15 men; mean age, 52.9 years; age range, 22-90 years). By the consensus of two observers, the precentral gyri, postcentral gyri, and superior frontal cortex (SFC) were identified based on the established anatomical methods. The SI of the SWM in the precentral and postcentral gyri on PADRE images was divided into three grades in comparison with that of the SFC: Grade I, isointense; Grade II, slightly hypointense; and Grade III, markedly hypointense. Results The SWM in the precentral and postcentral gyri showed hypointensity on PADRE images. In the SI analyses of the PADRE images, the Grade I, Grade II, and Grade III appearances were found in one (1%), 20 (23%), and 65 (76%) of the 86 precentral gyri (43 subjects), respectively, and in one (1%), 23 (27%), and 62 (72%) of the 86 postcentral gyri, respectively. Conclusion On PADRE images, the perirolandic SWM showed hypointensity compared to other cerebral cortices, which probably reflects differences in the concentrations of the nerve fibers, as well as the higher myelin content. PADRE may be useful for the identification of the central sulcus by assessing the SI of the SWM.

Functional cortical reorganization in cases of cervical spondylotic myelopathy and changes associated with surgery.

OBJECTIVE The physiological mechanisms underlying the recovery of motor function after cervical spondylotic myelopathy (CSM) surgery are poorly understood. Neuronal plasticity allows neurons to compensate for injury and disease and to adjust their activities in response to new situations or changes in their environment. Cortical reorganization as well as improvement in corticospinal conduction happens during motor recovery after stroke and spinal cord injury. In this study the authors aimed to understand the cortical changes that occur due to CSM and following CSM surgery and to correlate these changes with functional recovery by using blood oxygen level-dependent (BOLD) functional MRI (fMRI). METHODS Twenty-two patients having symptoms related to cervical cord compression due to spondylotic changes along with 12 age- and sex-matched healthy controls were included in this study. Patients underwent cervical spine MRI and BOLD fMRI at 1 month before surgery (baseline) and 6 months after surgery. RESULTS Five patients were excluded from analysis because of technical problems; thus, 17 patients made up the study cohort. The mean overall modified Japanese Orthopaedic Association score improved in patients following surgery. Mean upper-extremity, lower-extremity, and sensory scores improved significantly. In the preoperative patient group the volume of activation (VOA) was significantly higher than that in controls. The VOA after surgery was reduced as compared with that before surgery, although it remained higher than that in the control group. In the preoperative patient group, activations were noted only in the left precentral gyrus (PrCG). In the postoperative group, activations were seen in the left postcentral gyrus (PoCG), as well as the PrCG and premotor and supplementary motor cortices. In postoperative group, the VOA was higher in both the PrCG and PoCG as compared with those in the control group. CONCLUSIONS There is over-recruitment of sensorimotor cortices during nondexterous relative to dexterous movements before surgery. After surgery, there was recruitment of other cortical areas such as the PoCG and premotor and supplementary motor cortices, which correlated with improvement in dexterity, but activation in these areas was greater than that found in controls. The results show that improvement in dexterity and finer movements of the upper limbs is associated with recruitment areas other than the premotor cortex to compensate for the damage in the cervical spinal cord.