Dysgraphia disorder forecasting and classification technique using intelligent deep learning approaches.

Writing abilities are impacted by dysgraphia, a condition of learning disability. It might be challenging to diagnose dysgraphia at an initial point of a child's upbringing. Problematic abilities linked to Dysgraphia difficulties that is utilized in detecting the learning disorder. The features used in this research to identify dysgraphia include handwriting and geometric features that is reclaimed using kekre-discrete cosine mathematical model. The feature learning step of deep transfer learning makes good use of the obtained features to identify dysgraphia. The results of the data collection indicate that this study can use handwritten images to detect children who have dysgraphia. Compared to past investigations, this experiment has shown a significant improvement in the capacity to identify dysgraphia using handwritten drawings. The proposed approach is compared with the machine learning and deep learning approaches where the Kekre-Discrete Cosine Transform with Deep Transfer Learning (K-DCT-DTL) outperforms the existing approaches. The proposed K-DCT-DTL approach attains 99.75% of highest accuracy that exhibits the efficiency of the proposed method.

Progressive macrographia for block letter writing: A case study.

"Macrographia", a relatively rare symptom generally following cerebellar diseases, consists of an abnormally large handwriting. The case reported in the present investigation shows several outstanding features. First, it is of the progressive variety, letters increase in size as one goes through the word towards the lower-right portion of space. Moreover, it is limited to one allographic variety, that is, block letters. This phenomenon is previously unreported, all allographic varieties being usually equally affected. Finally, no prominent cerebellar or basal ganglia abnormality could be demonstrated with structural MRI or PET. From a cognitive point of view, a peculiar combination of spatial attention, executive function and working memory deficits is proposed to account for the progressive misalignment and elongation of individual letters when specifically writing in block prints. From an anatomical perspective, the pattern of multifocal lesions, encompassing multiple cortical areas in both hemispheres and the corpus callosum, may support this multi-componential interpretation of the reported phenomenon.

Developmental dysgraphia is often associated with minor neurological dysfunction in children with developmental coordination disorder (DCD).

OBJECTIVES: Children with developmental coordination disorder (DCD) are particularly affected by handwriting disorders, which remain poorly understood and are not clearly defined. The aim of our study is to provide a better understanding of handwriting disorders, and specifically of dysgraphia in children with DCD. METHODS: Sixty-five children with DCD (5-15 years), enrolled according to DSM-5, were assessed with handwriting testing and standardized assessments of neuropsychological, neurovisual, MRI and neuropsychomotor functions, with special attention paid to muscular tone examination. RESULTS: While handwriting disorders were strongly represented in our sample of children with DCD (89%), dysgraphia appeared uncommon (17%) and was closely related to several specific dysfunctions of laterality establishment; mild pyramidal tract dysfunction with distal phasic stretch reflex (PSR) in lower limbs; digital praxis slowness (both P<0.05). DISCUSSION: In our sample, dysgraphia was closely related to minor neurological dysfunction (MND) suggesting a disturbance of motor control at the level of the corticospinal motor pathway. This highlights the uncommon character of dysgraphia in children with DCD for which diagnosis should be made through a particular attention to evaluation of MND with muscular tone examination. This consideration, both in the research setting and in clinical practice, appears necessary to avoid inaccurate clinical diagnosis and to optimize appropriate therapeutic management.

Agraphia with reversible splenial corpus callosum lesion caused by hypoglycemia.

BACKGROUND: Neurological manifestations caused by hypoglycemia range from reversible focal deficits and transient encephalopathy to irreversible coma or death. Recently, high signal intensity lesions in the splenium of the corpus callosum on diffusion-weighted magnetic resonance imaging were reported in adults experiencing hypoglycemia. However, patients presenting with agraphia are rare. SUBJECT AND METHODS: We examined a 17-year-old left-handed female patient with type 1 diabetes who exhibited transient left agraphia with a reversible splenium lesion of the corpus callosum on diffusion-weighted imaging caused by hypoglycemia, which was improved with blood glucose management alone. CONCLUSION: This rare case indicates that agraphia, a sign of callosal disconnection syndrome, can result from a reversible splenial lesion of the corpus callosum caused by hypoglycemia.

Molecular neuroimaging in primary progressive aphasia with predominant agraphia.

A 62-year-old male presented with progressive isolated writing and spelling difficulties. Neurological, neuropsychological, speech, and language evaluations identified only minimal additional abnormalities. The presenting characteristics did not meet criteria for any particular variant of primary progressive aphasia; his clinical presentation is best described as primary progressive aphasia, with a predominant, almost pure agraphia. Brain MRI showed asymmetric, bilateral parenchymal volume loss, with left hippocampal atrophy. Fluorodeoxyglucose-F18 positron emission tomography showed hypometabolism in the lateral left frontal lobe, including Exner's area. Beta-amyloid and tau-positron emission tomography scans were negative, indicating the etiology was not Alzheimer's disease. The underlying neurodegenerative process is most likely related to TDP-43, although a 4-repeat tauopathy cannot be excluded. Following his clinical evolution, and ultimately identifying the underlying pathology from autopsy, will elucidate the etiology of this interesting clinical presentation.

Unilateral Apraxic Agraphia without Ideomotor Apraxia from a callosal lesion in a patient with Marchiafava-Bignami disease.

Apraxic agraphia can be caused by left hemispheric cerebral lesions in the area that contains the spatial representations of the movements required to write, from a lesion in, or connections to, the frontal premotor cortex that converts these spatial representations to motor programs (Exner's area).  A right-handed woman with Marchiafava Bignami disease and lesions of the genu and splenium of her corpus callosum had apraxic agraphia without ideomotor apraxia of her left. A disconnection of Exner's area in the left hemisphere from the right hemisphere's premotor and motor areas may have led to her inability to write with her left hand.

The neural substrates of improved phonological processing following successful treatment in a case of phonological alexia and agraphia.

Phonological deficits are common in aphasia after left-hemisphere stroke, and can have significant functional consequences for spoken and written language. While many individuals improve through treatment, the neural substrates supporting improvements are poorly understood. We measured brain activation during pseudoword reading in an individual through two treatment phases. Improvements were associated with greater activation in residual left dorsal language regions and bilateral regions supporting attention and effort. Gains were maintained, while activation returned to pre-treatment levels. This case demonstrates the neural support for improved phonology after damage to critical regions and that improvements may be maintained without markedly increased effort.

The oral spelling profile of posterior cortical atrophy and the nature of the graphemic representation.

Spelling is a complex cognitive task where central and peripheral components are involved in engaging resources from many different cognitive processes. The present paper aims to both characterize the oral spelling deficit in a population of patients affected by a neurodegenerative condition and to clarify the nature of the graphemic representation within the currently available spelling models. Indeed, the nature of graphemic representation as a linear or multi-componential structure is still debated. Different hypotheses have been raised about its nature in the orthographic lexicon, with one positing that graphemes are complex objects whereby quantity and identity are separately represented in orthographic representations and can thus be selectively impaired. Posterior cortical atrophy (PCA) is a neurodegenerative condition that mainly affects visuoperceptual and visuospatial functions. Spelling impairments are considered part of the disease. Nonetheless the spelling deficit has received little attention so far and often it has been interpreted in relation to peripheral impairments such as writing difficulties associated with visuoperceptual and visuospatial deficits. In the present study we provide a detailed characterization of the oral spelling profile in PCA. The data suggest that multiple deficits underpin oral spelling problems in PCA, with elements of surface and phonological dysgraphia but also suggesting the involvement of the graphemic buffer. A large phenotypic individual variability is reported. Moreover, the larger proportion and the specific nature of errors involving geminate (i.e., double) as compared to non-geminate (i.e., non-double) letters suggest that a further central impairment might be associated with the abstract graphemic representation of letter numerosity. The present study contributes to the clinical characterization of PCA and to the current debate in the cognitive literature on spelling models; findings, despite not definitive, support the hypothesis that graphemic representations are multidimensional mental objects that separately encode information about grapheme identity and quantity.

Cerebellum and apraxia.

As early as the beginning of the nineteenth century, a variety of nonmotor cognitive and affective impairments associated with cerebellar pathology were occasionally documented. A causal link between cerebellar disease and nonmotor cognitive and affective disorders has, however, been dismissed for almost two centuries. During the past decades, the prevailing view of the cerebellum as a mere coordinator of autonomic and somatic motor function has changed fundamentally. Substantial progress has been made in elucidating the neuroanatomical connections of the cerebellum with the supratentorial association cortices that subserve nonmotor cognition and affect. Furthermore, functional neuroimaging studies and neurophysiological and neuropsychological research have shown that the cerebellum is crucially involved in modulating cognitive and affective processes. This paper presents an overview of the clinical and neuroradiological evidence supporting the view that the cerebellum plays an intrinsic part in purposeful, skilled motor actions. Despite the increasing number of studies devoted to a further refinement of the typology and anatomoclinical configurations of apraxia related to cerebellar pathology, the exact underlying pathophysiological mechanisms of cerebellar involvement remain to be elucidated. As genuine planning, organization, and execution disorders of skilled motor actions not due to motor, sensory, or general intellectual failure, the apraxias following disruption of the cerebrocerebellar network may be hypothetically considered to form part of the executive cluster of the cerebellar cognitive affective syndrome (CCAS), a highly influential concept defined by Schmahmann and Sherman (Brain 121:561-579, 1998) on the basis of four symptom clusters grouping related neurocognitive and affective deficits (executive, visuospatial, affective, and linguistic impairments). However, since only a handful of studies have explored the possible role of the cerebellum in apraxic disorders, the pathophysiological mechanisms subserving cerebellar-induced apraxia remain to be elucidated.

Progressive apraxic agraphia with micrographia presenting as corticobasal syndrome showing extensive Pittsburgh compound B uptake.

A 65-year-old woman developed progressive apraxic agraphia, characterized by poorly formed graphemes, a kanji (Japanese morphograms) recall impairment, relatively preserved oral spelling of kanji characters, and incorrect stroke sequences on writing accompanied by micrographia over a 3-year period. She also showed minor degrees of rigidity, limb-kinetic apraxia, and ideomotor apraxia of the left hand. Although asymmetric rigidity and limb-kinetic apraxia strongly suggested corticobasal degeneration, (11)C-Pittsburgh compound B positron emission tomography (PiB-PET) showed the predominantly right-sided accumulation of amyloid ß in the cortices and striatum. (18)F-fluoro-deoxy-glucose PET and single photon emission computed tomography with a (99m)Tc-ethylcysteinate dimer (ECD-SPECT) also revealed predominantly right-sided hypometabolism and hypoperfusion in the primary sensorimotor cortex, posterior cingulate gyrus, temporoparietal cortices, frontal cortices, thalamus, and basal ganglia, a pattern characteristic of both corticobasal degeneration and Alzheimer's disease. The findings suggest that progressive apraxic agraphia with micrographia presenting as corticobasal syndrome can show an Alzheimer's disease pathology. It is also suggested that ideomotor apraxia of the left hand can occur without a callosal lesion, and is caused by hypometabolism or hypoperfusion in the right frontal and parietal cortices, as revealed by PET and SPECT.

"Apraxic dysgraphia" in a 15-year-old left-handed patient: disruption of the cerebello-cerebral network involved in the planning and execution of graphomotor movements.

Apraxic agraphia is a peripheral writing disorder caused by neurological damage. It induces a lack or loss of access to the motor engrams that plan and programme the graphomotor movements necessary to produce written output. The neural network subserving handwriting includes the superior parietal region, the dorsolateral and medial premotor cortex and the thalamus of the dominant hemisphere. Recent studies indicate that the cerebellum may be involved as well. To the best of our knowledge, apraxic agraphia has not been described on a developmental basis. This paper reports the clinical, neurocognitive and (functional) neuroimaging findings of a 15-year-old left-handed patient with an isolated, non-progressive developmental handwriting disorder consistent with a diagnosis of "apraxic dysgraphia". Gross motor coordination problems were objectified as well but no signs of cerebellar, sensorimotor or extrapyramidal dysfunction of the writing limb were found to explain the apraxic phenomena. Brain MRI revealed no supra- and infratentorial damage but quantified Tc-99m-ECD SPECT disclosed decreased perfusion in the anatomoclinically suspected prefrontal and cerebellar brain regions crucially involved in the planning and execution of skilled motor actions. This pattern of functional depression seems to support the hypothesis that "apraxic dysgraphia" might reflect incomplete maturation of the cerebello-cerebral network involved in handwriting. In addition, it is hypothesized that "apraxic dysgraphia" may have to be considered to represent a distinct nosological category within the group of the developmental dyspraxias following dysfunction of the cerebello-cerebral network involved in planned actions.

Dysgraphia in Korean patients with Alzheimer's disease as a manifestation of bilateral hemispheric dysfunction.

BACKGROUND: In writing, linguistic (i.e., spelling) and nonlinguistic (i.e., arranging strokes or letters) functions are processed by the left and right hemispheres, respectively. The configuration of Korean alphabet, 'Hangul' invokes nonlinguistic, visuospatial functions that other writing systems use less extensively. Patients with Alzheimer's disease (AD) have bilateral involvement of temporoparietal-frontal areas that are responsible for processing language and visuospatial functions. OBJECTIVES: The aim of this study was to examine the nature of Hangul writing dysfunction, which may be associated with bilateral hemispheric impairments in AD. METHODS: A sample of 75 patients with AD and 20 healthy controls (HC) performed a Hangul writing task. Neuroimaging positron emission tomography (PET) data of 22 patients were utilized to measure the regional brain glucose metabolism associated with Hangul writing. RESULTS: The writing performance of the AD group was significantly reduced and different types of errors were observed as the disease got worse. Glucose hypometabolism correlated with Hangul writing impairment was located in the right occipitotemporal lobe and left temporoparietal lobe. CONCLUSIONS: The PET findings demonstrate that impairment in Hangul writing performance in Korean AD patients is closely related to a functional decline in both the right and left hemispheres. The study provides a unique contribution to the knowledge of dysgraphia in a non-alphabetical writing system as well as the underlying neuropathology of dysgraphic features in such languages.

Functional dissociation between Kana and Kanji: agraphia following a thalamic hemorrhage.

We report the case of a 61-year-old woman with a left thalamic hemorrhage causing agraphia of Kanji (morphograms). Single-photon emission computed tomography (SPECT) showed a decrease in the blood flow in the left thalamus from the superior temporal convolution to the parietal lobe, as well as in the frontal lobe while computed tomography showed no remarkable lesions in the cortex. The agraphia in this case may be due to the thalamic lesion itself, but the SPECT findings strongly suggest that a secondary cortical lesion may be involved in producing the higher cognitive disorder.

Isolated thalamic agraphia with impaired grapheme formation and micrographia.

Two patients with isolated thalamic agraphia are described. Both showed kanji (Japanese morphograms) agraphia due to impaired character recall, grapheme deformity and micrographia (progressive reduction in character size during writing) after a lesion that involved the ventral lateral and ventroposterolateral nuclei. Single photon emission computed tomography with a (99m)Tc-ethylcysteinate dimer revealed hypoperfusion in the left precentral gyrus (Brodmann Area 6) and anterior supramarginal gyrus in both. Six months later, the extent of blood flow reduction decreased in the supramarginal gyrus in both patients and the precentral gyrus in patient 1. By this time, the writing impairment improved to nearly the normal range. Our study suggests that kanji agraphia (corresponding to lexical agraphia in Western countries) with poor grapheme formation and micrographia arises from a lesion in the ventral lateral and ventroposterolateral nuclei in the left thalamus. The accompaniment of poor grapheme formation and micrographia may reflect disruption of the cortico-subcortical motor circuit involving the putamen, thalamus, premotor cortex and sensorimotor cortex. It is also suggested that multiple cortical sites can be a target for secondary dysfunction that yields agraphia in a thalamic lesion, and that the recovery of reduced cortical blood flow does not always proceed in parallel with that of agraphia.

Sporadic corticobasal syndrome with progranulin mutation presenting as progressive apraxic agraphia.

OBJECTIVE: To examine the relationship between progranulin gene mutation and apraxic agraphia. DESIGN: Case report. SETTING: Tertiary care medical center. PATIENT: A 49-year-old right-handed woman who presented with apraxic agraphia that progressed into the corticobasal syndrome. RESULTS: This woman had no family history of neurodegenerative disease. Magnetic resonance imaging and fluorodeoxyglucose positron emission tomographic scans of her head revealed significant asymmetric frontoparietal abnormalities, in keeping with the clinical diagnosis of corticobasal syndrome. Progranulin gene sequencing identified a 4-base pair deletion. CONCLUSIONS: Patients presenting with early apraxic agraphia, a progressive disease course, and asymmetric frontoparietal abnormalities on brain scans should be considered for progranulin gene testing despite negative family history.

Hanja (Ideogram) alexia and agraphia in patients with semantic dementia.

Posterior fusiform gyrus (BA 37) is responsible for Hanja (ideogram) alexia in stroke patients. Patients with semantic dementia (SD) have lesions in the basal temporal area. The close proximity in these two lesions and the fact that reading ideograms requires holistic processing as is necessary in recognition of objects, suggests a possibility that ideogram alexia/agraphia may occur in patients with SD. We established and carried out Hanja and Hangul (phonogram) reading/writing tasks on six SD patients and nine Alzheimer's disease (AD) patients as control to see if these two patient groups show dissociation in the two sets of tests. SPM analysis was performed on the SD patients' PET images to look for any dysfunctions in the posterior fusiform gyrus. The SD patients manifested Hanja alexia/agraphia whereas Hangul reading/writing ability was relatively preserved. There were group differences between SD and AD in the Hanja tasks but not in the Hangul tasks. The SPM analysis revealed no hypometabolism in the posterior fusiform gyrus, but only in the middle and the anterior part of the temporal gyrus. Dysfunction in the middle temporal gyrus (BA 21) may have disrupted the temporal lobe connections preventing the function of the posterior fusiform gyrus.

Agraphia in intellectually normal Japanese patients with ALS: omission of kana letters.

To investigate the occurrence of a writing defect, omission of kana letters (OKL), in intellectually normal Japanese patients with amyotrophic lateral sclerosis (ALS), and define the neuroimaging profile of OKL. Sixteen Japanese adults (10 men and 6 women), similar in age (mean 62.9 +/- 9.9 years) and level of education (mean 12.6 +/- 2.13 years), with early-stage, classical ALS (mean duration 15.9 +/- 5.45 months) were investigated, including tests of motor function and ALS progression; intellectual function including writing ability; and neuroimaging, with follow-up of 1 year. Main outcome measures were as follows: Raven's Colored Progressive Matrices (RCPM: intellect and psychomotor speed); one-minute verbal fluency measurement; paired associate word-learning test (PAWLT); Western Aphasia Battery (WAB); moraic segmentation test; magnetic resonance imaging (MRI); and (123)I-isopropyl amphetamine ((123)I-IMP) or (99m)Tc-ethylcysteinate dimmer (ECD) single photon emission tomography (SPECT). Three patients (18.8%) showed OKL (WAB), with disturbance in moraic segmentation. One patient showed decreased blood flow to the bilateral frontal lobes by (123)I-IMP-SPECT. Patients with OKL did not differ significantly from those without in the RCPM (intellect), RCPM (time), verbal fluency, or PAWLT (p = 0.10, 0.84, 0.63, 0.55). Although motor dysfunction and weakness progressed during follow-up, none developed symptoms of dementia. The OKL may develop as a relatively early cognitive symptom in intellectually normal Japanese patients with classical ALS. The neuroimaging profile of OKL remains uncertain.

Alternative psychosis and dysgraphia accompanied by forced normalization in a girl with occipital lobe epilepsy.

An 11-year-old girl who had been given antiepileptic drugs (AEDs) for occipital lobe epilepsy was hospitalized with alternative psychosis and dysgraphia accompanied by forced normalization of the EEG. Her epileptic seizures and psychosis disappeared after administration of carbamazepine. She developed dysgraphia for Kanji words (Japanese morphograms). The EEG showed sporadic spikes predominantly in the left occipital region, and [123I]iomazenil single-photon-emission computed tomography (IMZ-SPECT) imaging revealed an area of hypoperfusion in the left occipital lobe. Interestingly, the left posterior inferior temporal area is known to play an important role in writing Kanji words. It is assumed that abnormal discharges in the left occipital lobe were projected into the left posterior inferior temporal area and that a functional disorder in that area led to dysgraphia; however, further exploration is needed.