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F Tamaru

Publications and source records attributed to F Tamaru.

14 recordsLinked to original sources

Disturbances in higher function in Parkinson's disease.

The most striking of the cognitive deficits in Parkinson's disease is 'subcortical dementia', which is similar to the cognitive deficits caused by frontal lobe damage. Of the several causes of the cognitive deficits in Parkinson's disease, the most interesting theoretical mechanism is the dysfunction of the cortical-basal ganglionic circuits connecting the frontal lobe and the basal ganglia. As the activity of these circuits can be modulated at the striatum by the nigrostriatal dopaminergic system, cognitive function can be influenced by the pathological change in the substantia nigra in Parkinson's disease. As a result of the dysfunction of this system, disturbances of memory, attention, and executive function occur. Our study found that the dopaminergic system plays a role in the disturbance of the set-shifting ability in Parkinson's disease.

Aged↗

[Analysis of gait disturbance in a patient with corticobasal degeneration].

A 64-year-old right-handed man was admitted because of increasing clumsiness of the right hand and difficulty in walking since 8 months earlier. The WAIS revealed verbal IQ 124, performance IQ 104 and full scale IQ 115. Neurological examination revealed slight dysarthria and normal eye movements. The right upper extremity showed Gegenhalten, tremor, dystonic elbow flexion, marked grasp reflex, grasping and groping behavior. Voluntary movements were slow and clumsy on the right side. However, neither ideational nor ideomotor apraxia was observed. Tendon reflexes were slightly exaggerated on the right side. Plantar responses were normal. The patient had difficulty in initiating forward walking and turning movements. Once started, he walked dragging his right foot ahead of the left with short steps. A line on the floor was of no benefit. He could not stride across the line on the floor in front of him. Analysis of gait with floor reaction force revealed that the single step rhythm of his frozen gait was about 1.5 Hz, which contrasted with the high frequency seen in Parkinson's disease. MRI demonstrated atrophy of the frontal and parietal lobes on both sides. 123I-IMP single-photon emission CT demonstrated severe hypoperfusion of the left frontal and parietal lobes. Frozen or shuffling gait is a popular symptom as well as unsteady gait and tendency to fall in corticobasal degeneration. It may result from the frontal lobe dysfunction. Lack of improvement in freezing by the visual input contrasts with Parkinson's disease and may be related to dysfunction of the mesial part of the frontal lobe or the parietal lobe involved in corticobasal degeneration.

Basal Ganglia Diseases↗

[Corticobasal degeneration: clinico-pathological studies on two cases].

We reported two patients with clinical features of corticobasal degeneration (CBD), one with autopsy observations. Their illness began in their sixties, ran progressive course and ended in death in about five years. The initial symptom was difficulty in manipulating with the left hands. Gradually the left lower limbs and the right limbs were also involved and the left became useless. They developed Parkinsonism, myoclonus, dystonia, hyperreflexia and vertical gaze palsy. They also showed the dysfunction of the fronto-parietal cortices, including grasping reflex, motor neglect, hemispatial neglect, constructional disturbance and cortical sensory loss. Dementia did not manifest until the terminal stage. Neuro-radiological studies demonstrated mild dilatation of the right central sulcus and marked reduction in cerebral blood flow in the fronto-parietal cortices, predominant in the right. Pathological examination in one of the case confirmed the the clinical diagnosis of CBD. There was a neuronal loss affecting second and third layers of the fronto-parietal cortices, especially the right parasylvian region, associated with spongiosis in these laminae and marked gliosis in deeper layers. Swollen, poorly staining (achromatic) neurons were observed in fifth layer. The hippocampus was unaffected. In the substantia nigra, there was extensive loss of pigmented cells. No Pick bodies, senile plaques, neurofibrillary tangles were observed in any region of the brain. The initial manifestations of their illness, the motor disturbances in the left upper extremities, were distinctive features in our patients. We could find no detailed description of these symptoms in the literature. We analysed these manifestations and described the results.(ABSTRACT TRUNCATED AT 250 WORDS)

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Event-related potentials, reaction time, and cognitive state in patients with Parkinson's disease.

ERPs, RT, and cognitive state in 53 patients with PD were studied. The peak latency of P300 and the RT in PD patients were significantly prolonged in the advanced stage of illness. The cognitive state in PD patients was characterized by impairment of attention, recent memory, and constructional ability in categories of the Folstein Mini-Mental State Examination. The significant association between neurophysiological and neuropsychological measurements suggests that these measurements reflect a disrupted aspect of cognitive function in PD patients.

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[A case of Cheyne-Stokes respiration with cyclic mutism during apneic period].

A 77-year-old man showed Cheyne-Stokes respiration (CSR) without a consciousness disturbance. In each apneic period of CSR, he became mute. In the apneic and mute state, he could open his mouth or protrude his tongue, but he could not breath or speak. In this patient, it was evident that not only phonation but also speech was under the control of respiration. Neuroimaging technique revealed an infarction in the right anterior cingulate gyrus and supplementary motor area as well as the entire perfusion area of the right middle cerebral artery. Marked atrophy of bilateral cerebral hemispheres was also observed. In this case, destruction of the right cingulate gyrus was thought to manifest occult functional fluctuation of the left cingulate gyrus influenced by the respiratory control mechanisms. This case suggested that the limbic system integrates the speech mechanism and the respiratory mechanism.

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[A case of progressive supranuclear palsy dramatically improved with L-threo-3,4-dihydroxyphenylserine].

We report a 67-year-old female with progressive supranuclear palsy (PSP) who dramatically improved when given L-threo-3,4-dihydroxyphenylserine (L-DOPS). This patient developed dysarthria, lack of facial expression, and slowness at age 64. She was admitted to a local hospital, diagnosed as having parkinsonism and treated with antiparkinsonian drugs. Despite this treatment, she had difficulty in turning over in bed and standing up from a seat, and began to fall backward at age 65. One year later, she had trouble in walking due to frequent falls and became bedridden. The patient was admitted to our hospital in July 1991 under treatment with 20 mg/200 mg of carbidopa/L-dopa and 4 mg of trihexyphenydyl hydrochloride per day. Neurological examination revealed masked face, pseudobulbar palsy, and dystonic rigidity of the neck and upper trunk. Eye movements were normal except for impaired vertical saccades and convergence inability. Deep tendon reflexes were generally brisk and the plantar responses were flexor bilaterally. Tests of pulsion showed that her postural reflex was markedly disturbed, especially in retropulsion. Her gait showed severe unsteadiness. Neuropsychological tests showed intellectual impairment, frontal lobe dysfunction, and memory disturbance. Computed tomography showed an atrophic midbrain with prominent enlargement of ambient and quadrigeminal plate cisterns. Single photon emission computed tomography (SPECT) using 123-I-isopropyl-iodoamphetamine demonstrated marked frontal hypoperfusion. L-DOPS was administered at a dose of 100 mg per day and gradually increased up to 600 mg per day over a period of five weeks, while carbidopa/L-dopa and trihexyphenidyl hydrochloride were continued as on admission.(ABSTRACT TRUNCATED AT 250 WORDS)

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[A case of midbrain and thalamic infarction showing Collier's sign in one side and blepharoptosis in the other side].

A 68-year-old man was admitted to the hospital complaining of aphasia and right hemiparesis. Neurological examination revealed aphasia, right hemiparesis and ataxia in the left upper extremity. He showed striking ocular symptoms: intense retraction of the right eyelid (Collier's sign), complete ptosis of the left eyelid which might conceal Collier's sign, marked upward gaze palsy and slight downward gaze palsy. Vertebral angiography and MRI revealed an infarction in the left medial area and the left crus cerebri in the upper midbrain, the left subthalamic area inferomedially extending from the adjacent area to the posterior commissure and the medial area in the left thalamus resulting from occlusion of the left mesencephalic artery. From these MRI findings and the reports on pathological findings of patients with Collier's sign, we suggest that damage in the posterior commissure or its adjacent area may be responsible for the sign. Upward gaze palsy is often associated with Collier's sign because fibers mediating upward gaze may decussate in the posterior commissure. Third nerve palsy is also associated with the Collier's sign in some patients. The mechanism creating Collier's sign may be a disturbance of inhibitory fibers leading to the motoneuron pool of the levator muscle in the posterior commissure or its adjacent area.

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Bradykinesia in Parkinson's disease: disorders of onset and execution of fast movement.

Simple reaction time lengthens in parkinsonian patients as the severity of motor disorder progresses. Shortening of reaction time was obtained by giving a warning signal to a greater extent in cases with severer motor disability. The results suggest that inattention, one of several symptoms common to lesions in the frontal lobe and Parkinson's disease, may be a factor in bradykinesia in purposive movements in the disease. The Wisconsin card sorting test and criterion shift task which we devised to deal with a single patients have difficulty in dealing with multiple sets simultaneously, which may be caused also by inattention. In execution of ballistic movement in parkinsonian patients, only a small torque constant in amount and in time can be produced in the beginning, irrespective of the size of force required, and subsequently enough force is built up to reach the target. This was more marked in cases with severe motor disability and in cases with decrease in power. Rigidity, mechanical properties of the limb or disorders in ocular movement were not responsible for the production of the initial small torque. Oculo-manual incoordination in visuomotor tracking tasks is also discussed.

Adult↗

Auditory agnosia. Analysis of a case with bilateral subcortical lesions.

We report a case of typical auditory agnosia. It is unique in that the clinical picture began with generalized auditory agnosia for verbal and nonverbal sounds and changed, over a period of two months, to a restricted auditory agnosia, confined to the recognition of nonverbal sounds. The lesions, confirmed by CT scanning and MRI, were subcortical bilaterally, without evidence of cortical damage, and have not previously been described. The results of audiological studies on temporal discrimination were similar to those described for bilateral temporal lobe lesions. The relationships between click intervals and the threshold to detect sound, and between numbers of clicks and the threshold, were also examined. We observed a tendency for the threshold to decline as the number of clicks was increased or the interval between two clicks was shortened. These phenomena are similar to temporal summation in cellular neurophysiology and we speculate that this phenomenon is an important factor in the auditory disturbances shown by the present case.

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Disappearance of sleep apnea by tracheal intubation in Creutzfeldt-Jakob disease.

We have described a patient with Creutzfeldt-Jakob disease who showed disappearance of sleep apnea by tracheal intubation. All night polygraphic study revealed a clear correlation between the cyclic EEG change and sleep apnea. The periodic synchronous discharge (PSD) phase in EEG corresponded to the breathing phase in respiration and non-PSD phase corresponded to the apneic phase. Intratracheal intubation has completely stopped both the apnea and the cyclic EEG change. Therefore, we assumed that the PSD-non-PSD cycle in EEG might causally relate with the peripheral obstruction of the airway during sleep.

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