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Query: UMLS:C0003635 (apraxia)
 2,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper presented a case of a right-handed male who showed a right hemiplegia without aphasia and apraxia. He lost the ability to write with the left hand. A 56-year-old right-handed man, who had a daughter of left-handedness, was sent to our hospital with a homonymous hemianopsia, facial weakness, spastic hemiparesis and sensory disturbance in the right side. CT scan revealed an infarction in the territory of the left middle cerebral artery. On a month after the onset, he was alert and oriented. His speech was normal and verbal comprehension was intact. Although he neglected the right side of the page, he could read and comprehend it correctly. In contrast with his normal abilities to speak, comprehend, and read, difficulties in writing were prominent. Spontaneous writing with the left hand was extremely poor, and he even had difficulty writing his own name. His dictation was also poor, but his writing improved with copying letters. Agraphia had seen even after USN was recovered. Analysis of this case suggested the presence of the dominance for speech, comprehension, and praxis in the intact right hemisphere, and writing center in the damaged left hemisphere.
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PMID:["Left unilateral agraphia with right hemiparesis" after occlusion of the left middle cerebral artery]. 141 44

We report a case with "releasing phenomenon of well learned praxis" with right hand caused by cerebral infarction in the territory of left anterior cerebral artery. A 71-year-old right-handed woman suddenly developed motor paralysis in right lower and upper limbs associated with mutism. Motor paralysis of the right upper limb and speech disturbance improved gradually. At this period it was noted that she grasped and used an object in front of her with right hand against her own will. The neurological findings about one month after the onset of the disease revealed very mild weakness of the right upper extremity and severe motor paralysis of the right lower limb. In addition, tendon reflex was exaggerated in the right lower limb and sensory disturbance was noted in the region distal from the right knee. Neuropsychologically, ideomotor apraxia was observed in the left hand. Pathological gasping of the right hand was also noted. When the patient saw and touched an object, she used it with her right hand against her own will, and her left hand voluntarily hindered the right hand. This behavior is apparently similar with the "compulsive manipulation of tools" reported previously. However, the following hitherto unknown phenomena were observed in the present patient: Her right hand performed pantomimic movement for the use of objects orally described by the examiner without visually presenting them. The right hand also tended to imitate the gestures of the examiner automatically, even if the patient was not asked for imitating the gestures. These behavioral abnormalities of the right hand was thought to be liberated from the inhibition system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Releasing phenomenon of well learned praxis with right hand]. 193 60

Higher cerebral dysfunctions such as aphasia, apraxia and agnosia have seldom been reported in multiple sclerosis (MS). 12 year-old right-handed boy felt unsteadiness of the body and headache for several days. Two months later, he had the same episode and complained of visual disturbance, and weakness and sensory disturbance on the face and the extremities. Additionally, he showed amnestic aphasia, acalculia, ideomotor apraxia, finger agnosia and right-left disorientation. Cerebrospinal fluid examinations revealed increases IgG, myelin basic protein and neuron specific enolase (11%, 25 ng/ml and 28.8 ng/ml, respectively). X-ray CT scan and MRI-CT examinations revealed sclerotic lesions on the left parietal white matter and the right mid-brain. The diagnosis was made as MS. He was treated with m-PSL (methyl-prednisolone) pulse therapy for three weeks and consecutively treated with PSL for four weeks. He recovered gradually, but visual disturbance and facial palsy remained. After seven months MRI-CT showed a high signal intensity on the left parietal white matter in spite of the disappearance of the lesion on X-ray CT scan. We suggest that these higher cerebral dysfunctions may result from the lesion of the left parietal white matter which produces a disconnection between each cortical area.
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PMID:[Multiple sclerosis with higher cerebral dysfunction: a case report]. 199 97

Somatosensory and motor functions of both hands were examined in 10 patients with unilateral parietal cortex lesions as revealed by computerized tomography. Tests of elementary somatosensory functions comprised surface sensibility, vibration, and position sense. For evaluation of complex somatosensory functions, the recognition of surface textures and object forms was tested. Motor performance was examined by measuring force and position control as well as manipulative and explorative motor behaviour. All patients showed varying degrees of sensory disturbance. Although the patients had no or minor paresis, they all had motor deficits concerning force control, fine movements, and manipulation with the hand contralateral to the lesion. Patients with more posteriorly located parietal lesions revealed predominantly severe disturbances of complex sensibility, precision grip, manipulation, and explorative finger movements. The characteristic and consistent feature of the disturbed motor behaviour was the loss of the purposive nature of the motor acts which were no longer adequate for the tasks (tactile apraxia). Paresis or ataxia could not account for this deficits.
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PMID:Role of the parietal cortex for sensorimotor transformation. Evidence from clinical observations. 275 92

The classical thalamic syndrome of Dejerine and Roussy is very rare. Sensory disorder are almost constant but the thalamic hyperpathia had not been reported. Clinical findings are reported in 14 patients with restricted lesions of the thalamus visible with the CT scan. Occasionally aphasia was found in patients with left sided lesion (with Thalamic Neglect, apraxia, mainly of ideomotor type and the so-called "Central Dazzle"). Thalamic lesions can produce a great variability of signs and symptoms.
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PMID:[Semeiologic aspects of circumscribed thalamic lesions. Clinico-tomodensitometric study]. 718 66

We studied the application of proton magnetic resonance spectroscopy (1H-MRS) in a case of corticobasal degeneration. A 73-year-old woman was referred to our hospital for dysarthria and clumsiness in right arm movement. Intelligence was normal and neither ideational apraxia or ideomotor apraxia were observed. Her speech was slurred and extremely slow. Neurological findings showed a limitation of ocular upward gaze movement, impaired smooth pursuit in the horizontal gaze, rigidity, limb kinetic apraxia and cortical sensory disturbance in the right arm. Magnetic resonance imaging (MRI) showed diffuse brain atrophy, especially in the left fronto-parietal cortex around the central sulcus. A positron emission tomography (PET) study showed diffuse decrement of cerebral blood flow, dominantly in the left hemisphere. The decrease in the uptake of 18F-Fluoro-deoxyglucose also revealed glucose hypo-metabolism, especially in the left frontal and parietal lobe. 1H-MRS by the multivoxel method showed a decrease in N-acetylaspartate (NAA)/Creatine to 1.0 in the left basal ganglia and temporal lobe, compared to the values between 1.4 and 1.7 in the right basal ganglia. These findings indicated that 1H-MRS might detect neuronal loss or degeneration when MRI showed minimal cortical atrophy. This study, the first application of 1H-MRS in a case of corticobasal degeneration, showed that this method was useful for the evaluation of pathophysiological changes in corticobasal degeneration.
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PMID:[A lateralized reduction of NAA in a case of corticobasal degeneration (CBD): application of proton magnetic resonance spectroscopy (1H-MRS)]. 962 63

To investigate clinicoanatomic correlations of higher brain dysfunctions in corticobasal degeneration, regional cerebral blood flow (rCBF) was semiquantitatively measured with single-photon emission computed tomography in 9 patients with corticobasal degeneration and 12 age-matched control subjects. The patients showed significant reductions of relative tracer uptake in widespread cortical areas, as well as the basal ganglia and thalamus. Interhemispheric difference of hypoperfusion was significant in the sensorimotor and posterior parietal cortices. Asymmetric limb apraxia and cortical sensory disturbance corresponded to either sensorimotor cortical or posterior parietal cortical hypoperfusion or both. Compared with the patients without dementia, those with dementia showed significant reductions of relative rCBF in the inferior prefrontal region in the more affected hemisphere. The unique correlation of cortical signs with regional hypoperfusion may be useful in distinguishing between corticobasal degeneration and other neurodegenerative diseases.
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PMID:Cerebral blood flow correlates of higher brain dysfunctions in corticobasal degeneration. 1061 66

A 41-year-old, right-handed man was admitted to our hospital on September 12, 2002, due to progressive clumsiness in both hands. The patient had been diagnosed as having multiple sclerosis three years prior to admission. He noticed difficulty in manipulating objects three months before admission. Cervical T2-weighted MRI showed a high signal intensity at the level of C3-4 which was enhanced on T1-weighted image with gadolinium. On admission, neurological examinations revealed impairment of dexterity, deep sensory disturbance, and astereognosis in both hands. The clumsiness of complex finger movements was predominant on the left side, and was exaggerated with the eyes closed in association with pseudoathetosis. After steroid therapy, his clumsy hands improved gradually. This type of clumsiness in multiple sclerosis had been described as useless hand syndrome by Oppenheim. In accordance with our case, useless hand syndrome has been reported to arise from high cervical (C2-4) lesions, mainly involving the posterior cord ipsilateral to the clumsy hand. Although the majority of reported cases with useless hand syndrome had other neurological complications, such as hemiparesis, tetraparesis, and truncal ataxia, our patient exhibited a pure form of useless hand syndrome. In addition, useless hand syndrome is usually unilateral, and bilateral useless hand syndrome is very rare. Clumsiness of fine finger movements with astereognosis in our patient is similar to numb clumsy hands or limb-kinetic apraxia due to cervical spondylosis or postcentral gyrus lesion, respectively. This indicates an important role of the high cervical posterior cord in conveying a kinesthetic sense necessary to guide fine finger movements. It should be kept in mind that high cervical lesions in multiple sclerosis causes clumsy hands mimicking limb-kinetic apraxia.
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PMID:[A case of multiple sclerosis with bilateral useless hand syndrome as a main clinical feature]. 1583 90

A 74-year-old, right handed man, developed insidiously with levitation and clumsiness of the right upper limb. His right arm tended to levitate spontaneously, when he was examined. He could put the elevated arm down on command, while the arm resumed to antigravity posture when his attention was diverted. His right arm also exhibited unwilled elevation when performing complex finger movements on the right side. He had a feeling of strangeness of the elevated limb, especially with the eyes closed. In addition to asymmetric limb-kinetic apraxia, combined sensations such as stereognosis were disturbed on the right side. Brain MRI showed high signal lesions predominantly in the left cerebral cortices and basal ganglia. SPECT with (123)I-IMP revealed asymmetric hypoperfusion, predominantly in the left medial frontal and parietal regions. Two months after the onset, levitation of the arm gradually disappeared, with the development of rapidly progressive dementia, frontal signs, dystonia and generalized myoclonus. The diagnosis of Creutzfeldt-Jakob disease (CJD) was made based on the clinical features and cerebrospinal fluid biomarkers. The early manifestation of the patient mimicked corticobasal degeneration which presents with arm levitation or alien hand syndrome. It is suggested that CJD can represent involuntary movements with higher brain dysfunction resembling corticobasal degeneration at the early stage of the illness. Although the underlying mechanism of arm levitation is still unknown, frontal disinhibition and parietal cortical sensory disturbance may contribute to the development of involuntary arm levitation in our patient.
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PMID:[A case of Creutzfeldt-Jakob disease presenting with arm levitation as an initial symptom]. 2534 14

Limb apraxia is a higher brain dysfunction that typically occurs after left hemispheric stroke and its cause cannot be explained by sensory disturbance or motor paralysis. The comparison of motor signals and visual feedback to generate errors, i.e., visuo-motor integration, is important in motor control and motor learning, which may be impaired in apraxia. However, in apraxia after stroke, it is unknown whether there is a specific deficit in visuo-motor temporal integration compared to visuo-tactile and visuo-proprioceptive temporal integration. We examined the precision of visuo-motor temporal integration and sensory-sensory (visuo-tactile and visuo-proprioception) temporal integration in apraxia after stroke by using a delayed visual feedback detection task with three different conditions (tactile, passive movement, and active movement). The delay detection threshold and the probability curve for delay detection obtained in this task were quantitative indicators of the respective temporal integration functions. In addition, we performed subtraction and voxel-based lesion-symptom mapping to identify the brain lesions responsible for apraxia and deficits in visuo-motor temporal integration. The behavioral experiments showed that the delay detection threshold was extended and that the probability curve for delay detection was less steep in apraxic patients compared to controls (pseudo-apraxic patients and unaffected patients), only for the active movement condition, and not for the tactile and passive movement conditions. Furthermore, the severity of apraxia was significantly correlated with the delay detection threshold and the steepness of the probability curve in the active movement condition. These results indicated that multisensory (i.e., visual, tactile, and proprioception) feedback was normally temporally integrated, but motor prediction and visual feedback were not correctly temporally integrated in apraxic patients. That is, apraxic patients had difficulties with visuo-motor temporal integration. Lesion analyses revealed that both apraxia and the distortion of visuo-motor temporal integration were associated with lesions in the fronto-parietal motor network, including the left inferior parietal lobule and left inferior frontal gyrus. We suppose that damage to the left inferior fronto-parietal network could cause deficits in motor prediction for visuo-motor temporal integration, but not for sensory-sensory (visuo-tactile and visuo-proprioception) temporal integration, leading to the distortion of visuo-motor temporal integration in patients with apraxia.
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PMID:Distortion of Visuo-Motor Temporal Integration in Apraxia: Evidence From Delayed Visual Feedback Detection Tasks and Voxel-Based Lesion-Symptom Mapping. 3021 Apr 34


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