Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ALEXIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2003

["Progressive acalculia": a variety of focal degenerative atrophy affecting number processing].

A 72-year-old man experienced increasing difficulties in calculating and processing numbers. He made many syntactic errors when he read and wrote numbers, both in arabic and number-word forms. Transcoding between arabic numerals and number-words was severely impaired. His calculation abilities were grossly impaired. He could not perform even simple multiplications, but additions and subtractions were preserved. He was unable to recite multiplication tables or the alphabet. In contrast, numerosity judgment, magnitude comparisons,and semantic evaluation of numbers were intact. The patient's deficit could be summarized as an Impairment in all tasks involving numbers in a verbal format, corresponding to the so-called "verbal anarithmetia'." It was noteworthy that verification of operations, including multiplications, was accurately performed. For example, the patient could not solve a multiplication like 8 x 9, but could estimate that 9 x 2=1 1 was closer to the exact result than 9 X 2=17, or could state that 8 x 2=16 was exact even though, at the same time, he expressed verbally the terms of the corresponding addition "eight plus two is ten." Other cognitive deficits were detected by neuropsychological tests which demonstrated mainly anomic aphasia, dysorthographic agraphia without alexia, impairment of short term and episodic memory, digital agnosia. However, the patient could not be considered to have demon-eti due to preserved self-sufficiency, except for tasks requiring calculation abilities. During the two years of follow-up, the impairment in processing numbers and calculation remained predominant over other deficits. Cerebral MRI showed an atrophy of the left temporal and parietal lobes, and SPECT study showed a reduction of regional cerebral blood flow of the left hemisphere. This original clinical presentation of a cerebral degenerative disease could be described as "primary progressive acalculia" whatever the underlying primary pathological process.

Aged↗
PubMedDate not supplied

[The neurobiology of developmental dyslexia: a survey].

One of the most common disorders affecting the ability to read is developmental dyslexia, which, unlike the alexia related to a loss of the capacity to read associated with brain damage, refers to a specific disorder in the acquisition of reading skills and becomes apparent in reiterated persistent difficulties in learning to read. A number of studies have attempted to detect structural and functional abnormalities that might be the origin of problems in learning to read. The use of functional neuroimaging techniques such as positron emission tomography (PET), spectroscopic magnetic resonance imaging (SMRI) and functional magnetic resonance imaging (fMRI) enables us to measure changes in the metabolic activity associated with alterations in the neuronal networks involved in the reading process. In this review, different studies are analysed in an attempt to identify alterations in the cortico subcortical regions which could be the origin of the developmental dyslexia. Results show that in dyslexics there is a temporoparietooccipital disconnection, and a disconnection with the left frontal cortex as regards the demands for fast auditory processing, as well as abnormalities in the connections between the temporoparietal cortex and the cerebellum with other regions of the brain. Such findings suggest that the altered areas of the brain do not only show a characteristic pattern of hypoactivation, but also that these alterations could be the cause of this malady. We highlight the importance of these findings in the diagnosis and rehabilitation of this population.

Dyslexia↗
PubMed2002

[Clinical analysis of 7 patients with Gerstmann syndrome secondary to cerebral vascular disease].

OBJECTIVE: To analyze clinical features of patients with Gerstmann syndrome (GS). METHODS: We retrospectively analysed the clinical manifestations of 7 patients (6 men and 1 woman) with GS secondary to cerebral vascular diseases and reviewed the literatures. RESULTS: The age ranged from 51 to 70 years with a mean of 70 years. They all had sudden onset and the tetrad of GS-finger agnosia, left-right disorientation, agraphia and acalculia, 3 patients accompanied by incomplete aphasia, 3 by anomic aphasia, 2 by alexia and 1 by constructional apraxia. Cranial computed tomographic scan showed low-density focus of the left parietal lobe in 6 cases and high-density focus of the left parietal lobe in 1 case. CONCLUSION: GS has the high value in localization and the lesion is mainly localized to angular gyrus of the dominant hemisphere.

Aged↗
PubMed1992

[Visual agnosia evolving to optic aphasia--a case study].

The underlying mechanism of visual agnosia and optic aphasia has not been fully elucidated, although a number of hypotheses have been proposed. Besides, the difference between these two conditions has been a matter of debate. We report here the result of neuropsychological evaluation in a case of associative visual agnosia evolving to optic aphasia. A 64-year-old right-handed patient was found to be disoriented and confused after undergoing the operation of gastrectomy. CT scan revealed a large infarction in the territory of left posterior cerebral artery. Since 3 weeks after onset, neuropsychological investigations were carried out during 5 months. He was alert and co-operative. Right homonymous hemianopia with macular sparing was noted, but his visual acuity was normal. There was neither a global deterioration of intellectual capacities nor aphasia. Most striking finding was his difficulty in identifying common objects and colours along with a profound alexia. Prosopagnosia was absent. Visual naming both for objects and line drawings was severely impaired. He was unable to describe or demonstrate the use of the objects which could not be named. Pointing to objects named by the examiner was also severely impaired. Although tactile naming was also impaired, both of auditory naming for environmental sounds and naming objects in response to verbal descriptions were preserved. While he was not able to copy the objects skillfully, matching of identical objects and matching objects to line drawings were normal. Clumsiness of coping was thought to be due to his constructional apraxia and visuomotor ataxia. Therefore, his deficit in visual domain was considered to be associative visual agnosia.(ABSTRACT TRUNCATED AT 250 WORDS)

Agnosia↗
PubMed1992

[A case of malignant glioma associated with verbal recent memory disturbance due to left hippocampal atrophy; case report].

Verbal recent memory disturbance was observed in a patient with a malignant glioma associated with left hippocampal atrophy. A 25 year-old male was admitted because of seizures. CT scan and MRI showed enhanced mass lesions in the left temporal lobe associated with ipsilateral hippocampal atrophy. Neurological examination disclosed right homonymous hemianopsia, word amnesia, alexia, agraphia and acalculia. Neuropsychological examination disclosed verbal recent memory disturbance, which consisted of impaired recall of the precisely memorized words after some interruption. Although hippocampal lesions are known to be often associated with cerebrovascular disease, hippocampal atrophy due to brain tumor is quite unusual. This case suggested that the left hippocampus is closely related to verbal recent memory. Hippocampal atrophy in this case conceivably derived from the decreased arterial flow due to perifocal edema or obstructive hydrocephalus.

Adult↗
PubMed2003

[Acute severe leukoencephalitis with posterior lesions due to Borrelia burgdorferi infection].

INTRODUCTION: Central nervous system manifestations represent 0.54 to 8% of neurological complication in Lyme disease. OBSERVATION: A 78-year-old woman presented a severe meningo-encephalitis with visual disorders (agnosia, alexia) progressing towards coma. Cranial magnetic resonance imaging revealed large areas of hypersignal T2 in the white matter of the lower, parieto-occipital lobes and left temporal lobe. The cerebrospinal fluid (CSF) contained 16 then 293 white corpuscles/mm3 of lympho-monocytes, increased protein level from 2.67 to 5.83 g/l and an increase in IgG index with oligoclonal distribution of IgG. Serological Elisa analysis for Lyme disease was slightly positive in blood (confirmed by western blot) but clearly in the CSF (IgG and IgM). Treatment with ceftriaxone followed by methylprednisolone provided clinical improvement 3 months later. DISCUSSION: Acute meningo-encephalitis is often benign, protein-like and of good prognosis: the gnosic visual disorders with posterior leukoencephalopathy are unusual. A blood level of specific antibodies slightly positive on Elisa at the early stage of the infection warrants confirmation by Western blot in the blood and by Elisa in the CSF. Additional corticosteroid therapy may be required in the severe forms that evoke acute disseminated encephalomyelitis.

Acyclovir↗
PubMedDate not supplied

Progressive supranuclear palsy with widespread cerebral lesions.

A 51-year-old woman with no history of any familial neurological diseases initially presented with numbness in her extremities, slowing of movements, comprehension deficit, memory disturbance, dyscalculia, muscle rigidity, hyperreflexia, Parkinsonian gait, increasing disorientation, left-right disturbance, finger agnosia, alexia, acalculia, apraxia, aspontaneity, euphoria, gait disturbance, aphasia, echolalia, and in the terminal stage, mutism, contracture of lower extremities and cachexia. She died of bronchopneumonia at the age of 55. The brain showed widespread cerebral lesions, consisting of nerve cell loss and neurofibrillary tangles in the frontal, parietal and occipital cortex, demyelination and gliosis in the frontal, parietal and occipital subcortical white matter in addition to the typical pathological findings of progressive supranuclear palsy (PSP): severe neuronal loss with gliosis and neurofibrillary tangles (NFTs) in the subthalamic nucleus, globus pallidus and substantia nigra. In conclusion, we present a case of PSP with unusual clinical features (extrapyramidal signs, frontal and parietal lobe syndromes without ophthalmoplegia) and neuropathologically widespread cerebral lesions in addition to the typical pathological findings of PSP. The differential diagnosis of PSP and Alzheimer's disease and other degenerative disorders is discussed.

Alzheimer Disease↗
PubMed2004

[A case of dementia with motor neuron disease associated with agraphia--the omission of kana letters].

We report a 55-year-old right-handed Japanese man with motor neuron disease and dysgraphia of kana letters. He was admitted to our hospital because of dysarthria and dysphasia. On admission, the results of general physical examination were within normal limits. Neurological examination revealed severe dysarthria, dysphasia, impaired movement of the tongue without fasciculation and slight distal muscle weakness in the bilateral upper limbs. There were no fasciculation of the muscle. Deep tendon reflexes were hyperactive without Babinski's signs. Sensation, coordination, and gait were normal. Neurophysiological studies demonstrated normal motor nerve conduction velocities and sensory action potential. The results of needle electromyography of the upper limbs were compatible with motor neuron disease (MND). Magnetic resonance imaging (MRI) showed atrophy of the bilateral temporal region of the brain. 99mTc-HMPAO SPECT (Single Photon Emission Computed Tomography) showed reduced uptake of tracer in the bilateral temporal region. On neuropsychological examination, his behavior was normal, and orientation and intelligence were also preserved, but his speech was severely impaired. Reading comprehension was slightly impaired. In regard to writing comprehension, he had no difficulty in copying of words though dictation was found to be impaired. He omitted one kana letter in a word. Agraphia is accompanied by various factors such as aphasia, dementia, agnosia, alexia. But in this case at least for early stage, agraphia existed without other higher cortical dysfunction. He did not show severe dementia in his early stage of his disease, but developed it later in the disease's progression. In this case, agraphia might be due to the atrophic changes in the temporal lobe.

Agraphia↗
PubMed2004

[Neuronal circuits of reading and writing in Japanese language].

Japanese writing system consists of two different types of letters, kana (phonogram) and kanji (morphogram). Various types of alexia with or without agraphia in the Japanese language cause specific type of kanji/kanja dissociation. Upon the neuropsychological analysis of these dissociations, we have proposed a hypothesis of dual neuronal circuits of reading and writing process. Subsequent PET activation studies upon normal subjects confirmed the hypothesis; semantic reading pathway via area 37 on the inferior border of the left temporal lobe and phonological reading pathway via middle portion of the left lateral occipital lobe.

Agraphia↗
PubMed2005

[A case of carbon monoxide poisoning by explosion of coal mine presenting as visual agnosia: re-evaluation after 40 years].

We re-evaluated a case of carbon monoxide poisoning presenting as visual agnosia who had been injured by explosion of Miike-Mikawa coal mine 40 years ago. In an early stage, his main neuropsychological symptoms were visual agnosia, severe anterograde amnesia, alexia, agraphia, constructional apraxia, left hemispatial neglect and psychic paralysis of gaze, in addition to pyramidal and extra pyramidal signs. At the time of re-evaluation after 40 years, he still showed visual agnosia associated with agraphia and constructional apraxia. Concerning visual agnosia, recognition of the real object was preserved, while recognition of object photographs and picture was impaired. Thus, this case was considered to have picture agnosia as he could not recognize the object by pictorial cues on the second dimensional space. MRI examination revealed low signal intensity lesions and cortical atrophy in the bilateral parieto-occipital lobes on T1-weighted images. Therefore, the bilateral parieto-occipital lesions are likely to be responsible for his picture agnosia.

Aged↗
PubMed2006

[Callosal disconnection syndrome due to acute disseminated enchephalomyelitis].

We have reported a very rare case of a patient with callosal disconnection syndrome due to acute disseminated enchephalomyelitis (ADEM). A 54-year-old right-handed woman developed sudden consciousness disturbance and fever after 2 weeks when she had common cold. She did not have a history of stuttering. On admission, the neurological finding showed consciousness disturbance, and exaggerated muscle stretch reflex in four extremities without meningeal irritation. The cerebrospinal fluid examination revealed the cell counts of 273/mm3, the protein of 348 mg/dl and the myelin basic protein 18.3 pg/ml. The brain MRI demonstrated a focal high signal intensity in the right cerebellar peduncle, right temporal lobe, left occipital lobe and corpus callosum on the T2-weighted and FLAIR images. The lesion of corpus callosum was the trunk and splenium, sparing the dorsal side of splenium. Her diagnosis was ADEM. The steroid pulse therapy (metylpredinisolone 1 g/day for 3 days) improved the consciousness disturbance. After 6 weeks from the onset, the neuropsycological examination was performed. The remarkable findings included pure alexia without color naming defects, the acquired stuttering and one-way disturbance of somesthetic transfer from the left hand to the right. This patient may contribute to the study of functional localization of the corpus callosum.

Apraxias↗
PubMed2007

Multisystem Proteinopathy

CLINICAL CHARACTERISTICS: Multisystem proteinopathy (MSP) is a genetically heterogeneous, multisystem degenerative disorder characterized by adult-onset proximal and distal muscle weakness (clinically resembling a limb-girdle muscular dystrophy syndrome), early-onset Paget disease of bone (PDB), and premature frontotemporal dementia (FTD). Muscle weakness progresses to involve other limb and respiratory muscles. PDB involves focal areas of increased bone turnover that typically lead to spine and/or hip pain and localized enlargement and deformity of the long bones; pathologic fractures occur on occasion. Early stages of FTD are characterized by dysnomia, dyscalculia, comprehension deficits, and paraphasic errors, with minimal impairment of episodic memory; later stages are characterized by inability to speak, auditory comprehension deficits for even one-step commands, alexia, and agraphia. Mean age at diagnosis for muscle disease is 43 years, PDB is 41 years, and FTD is 56 years. Dilated cardiomyopathy, amyotrophic lateral sclerosis, and Parkinson disease are now known to be part of the spectrum of findings associated with MSP. DIAGNOSIS/TESTING: The diagnosis of MSP is established in a proband with typical clinical findings and a heterozygous pathogenic variant in VCP, HNRNPA1, HNRNPA2B1, or SQSTM1 identified by molecular genetic testing. MANAGEMENT: Treatment of manifestations: Weight control to avoid obesity; physical therapy and stretching exercises to promote mobility and prevent contractures; occupational therapy and mechanical aids (canes, walkers, orthotics, wheelchairs) as needed for ambulation/mobility; surgical intervention for foot deformity and scoliosis as needed; respiratory aids when indicated; assisted living arrangements for muscle weakness and/or dementia; bisphosphonates to relieve pain and disability from PDB; social and emotional support; education regarding safety precautions. Surveillance: Echocardiogram and electrocardiogram with repeat cardiac evaluation every two to three years or earlier if symptomatic; annual pulmonary function studies; sleep studies as clinically indicated; annual alkaline phosphatase measurement; skeletal imaging as indicated for evaluation of PDB; neurologic and neuropsychological assessment every two to three years or more frequently as needed; multidisciplinary monitoring for respiratory, cardiac, musculoskeletal, and cognitive decline. GENETIC COUNSELING: MSP is inherited in an autosomal dominant manner. Most individuals diagnosed with MSP have an affected parent. Estimates based largely on VCP-MSP suggest that approximately 5% of individuals have a de novo pathogenic variant. Each child of an individual with MSP has a 50% chance of inheriting the MSP-related pathogenic variant. Marked intrafamilial variability may be observed among heterozygous family members, including differences in age at onset, severity, rate of progression, and the specific combination of manifestations. Once the MSP-related pathogenic variant has been identified in an affected family member, predictive testing for at-risk family members and prenatal/preimplantation genetic testing are possible.

Inclusion Body Myopathy with Early-Onset Paget Dis↗
PubMed1979

Effect of certain cerebral hemispheric diseases on dreaming.

Dreaming may be altered by cerebral hemispheric disease. A woman who sustained a probable left posterior cerebral artery thrombosis, with right homonymous hemianopsia and alexia, had virtual cessation of dreaming for at least 9 months. Four individuals with temporal lobe epilepsy experienced recurrent painful (frightening) dreams, which in two patients showed features identical to seizures. Sleep recordings showed abnormalities in all four, including rhythmic temporal epileptiform activity during REM sleep. Lesions in parieto-occipital loci may interfere with production of the visual imagery required for dreaming (negative symptom in the Jacksonian sense) while epileptic activity in temporal loci may produce painful repetitive dream imagery (positive symptom).

Adult↗
PubMed1989

[Lexical agraphia caused by left temporoparietal hematoma].

A patient presented with dysorthographia associated with amnestic aphasia due to a left temporo-parietal hematoma. Reading, copying, graphism of letters were normal. Dictation showed better results for logatomes and regular words, without orthographical difficulty, than for those with orthographical problems (ambiguous and irregular words). The overall features suggested a disorder of the lexical system in which orthography of words known to patients is present. The phonological pathway of phoneme-grapheme conversion was preserved since errors were usually phonologically correct. Initially it was possible to conclude to a disorder of the semantic value of words in their visual form. Oral spelling, auditory reading and written denomination also showed more errors for words of difficult orthography. This patient presented a disorder of visual representation of words. Comparison of this case with the few reported ones showed that the latter often had amnestic aphasia and differed from our case in the associated lexical or phonologic alexia. A common feature of the lesions is involvement of the left angular gyrus is right-handed patients.

Aged↗
PubMed1989

[Multi-infarct dementia clinically simulating dementia of Alzheimer type. A comparison with angular gyrus syndrome].

A 74-year-old right-handed man with multiple cerebral infarction who presented with dementia simulating dementia of Alzheimer type (DAT) is reported. He had been well until April 20, 1987 when he developed transient right hand palsy lasting overnight. Eleven days later, he became confused, disorientated, and amnestic. He was admitted to this hospital on June 8. Physical examination revealed hypertension (170/90mmHg). On neurological examination, his consciousness was clear but he was demented. He showed disorientation, amnesia, and urinary incontinence. His most prominent symptom was disturbance of speech, including fluent aphasia and alexia with agraphia. Additionally, he showed ideomotor apraxia, construction apraxia, right-left agnosia, finger agnosia, and acalculia. On July 9, he had a transient attack of right hemiplegia with confusion. The brain CT scan performed on admission was unremarkable except for cavum septi pellucidum and a small low density area in the right basal ganglia. However, single photon emission computed tomography (SPECT) by 123I-labeled N-isopropyl-p-iodoamphetamine disclosed hypoperfusion of the cerebral blood flow in the border zones of the temporoparietal and frontal lobes on the left. A follow-up brain CT scan taken one month later demonstrated low density in the new areas corresponding to hypoperfusion shown by SPECT. Although the clinical features of the present case resembled those of DAT, dementia in this case was regarded as the result of multiple cerebral infarction since it occurred acutely with mild motor deficits, and brain CT scans and SPECT showed lesions indicating focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[Pure agraphia. Apropos of 2 cases].

Pure agraphia is a disorder of written language without aphasia, alexia or apraxia. Its existence has long been disputed. We report 2 cases due to a left parietal hematoma. In the first patient, with a deep precuneate lesion, agraphia included disorders in handwriting and orthographic problems in copying or writing from dictation with the two hands. The second patient, with a lesion of the postero-inferior part of the left angular gyrus, made errors in choice and combination of letters during dictation, whereas these same letters were well-written and copying was normal. The first cases of pure agraphia were ascribed to frontal lesions and then confusional states. Current opinion tends to implicate parietal lesions of various types: superior or inferior, internal or external. Findings in the present 2 cases and those reported indicate that pure parietal agraphia is heterogeneous.

Aged↗
PubMed1987

[A case of subtentorial ventricular diverticulum accompanied with choroid plexus papilloma in the lateral ventricle].

Marked non-communicating hydrocephalus may rarely cause ventricular rupture producing either a dilated cystic cavity (ventricular diverticulum) or communication between ventricle system and subarachnoid space (spontaneous ventriculostomy). Ventricular diverticulum has been believed to be collection of cerebrospinal fluid which escaped beneath the pia mater after rupture of ependymal layers and cerebral parenchyma. We proposed herein to report a case of subtentorial ventricular diverticulum which accompanied with choroid plexus papilloma of the lateral ventricle. A nine year-old girl admitted to our hospital complaining of clumsiness of hands and walking, disability of reading, headache and vomiting. The neurological examination revealed alexia, papilledema, anisocoria, righ hemianopsia, weakness of right upper limb, and cerebellar ataxia. CT brain scan showed a large high density area at the trigone of the left lateral ventricle with non-communicating hydrocephalus and an extra-axial low density area in the posterior fossa. The medial space of the left trigone was especially ballooned and is just shifted above incisura tentoria by the tumor. The intraventricular tumor was totally removed by operation and proved to be benign choroid plexus papilloma microscopically. The subtentorial mass was confirmed to be a cyst contiguous to the medial trigone of the lateral ventricle, namely ventricular diverticulum. Three special features were recognized in this case. The first, this was the first example of ventricular rupture accompanied with tumor in the lateral ventricle reviewing all reports of both ventricular diverticulum and spontaneous ventriculostomy. The second, this ventricular diverticulum was not produced merely by hydrocephalus alone but mainly by direct effects of the tumor.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Diseases↗