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PubMed2002

Loss of postural reflexes in long-term occupational solvent exposure.

Inhalation of organic solvents has long been known to damage various nervous systems, including cerebellum, brainstem, and pyramidal tract. However, little is known about the damage of the dopaminergic system. We report two patients with occupational long-term solvent exposure who developed postural instability without other features of parkinsonism. The concentration of HVA in CSF was decreased and the retropulsion was dramatically improved after the administration of levodopa. These findings indicate that the nigrostriatal dopaminergic neurons were disturbed by chronic solvent exposure, resulting in the loss of postural reflexes.

Adult↗
PubMed2003

Clinicopathological study of two subtypes of Pick's disease in Japan.

We examined the clinical and neuropathological findings in 3 cases of Pick's disease with Pick bodies (PiD) and 7 cases of atypical Pick's disease without Pick bodies (aPiD). PiD and aPiD cases corresponded clinically to frontotemporal dementia and semantic dementia, respectively, based on the clinical diagnostic criteria of frontotemporal lobar degeneration. Brain CT showed that cerebral atrophy was accentuated at an early stage of the illness in the anterior portion of the frontal lobes in PiD cases and in the anterior portion of the temporal lobes in aPiD cases. Neuropathologically, PiD cases showed more circumscribed lobar atrophy than aPiD cases. Both PiD and aPiD cases revealed moderate to severe degeneration with neuronal loss and gliosis in the affected cerebral cortex and subcortical nuclei, but only aPiD cases had pyramidal tract degeneration. Immunohistochemical analyses demonstrated that tauopathy with phosphorylated tau accumulation in the Pick bodies in PiD cases, while aPiD cases showed ubiquitinopathy with ubiquitin accumulation in the intraneuronal and dendritic inclusions. These findings suggested that two subtypes of Pick's disease in Japan can be distinguished not only neuropathologically but also clinically based on differences in pathogenesis.

Aged↗
PubMed1993

Input-output organization of the ventrolateral nucleus of the thalamus.

Input-output organization of the ventrolateral nucleus (VL) of the thalamus was analyzed electrophysiologically and morphologically at the single cell level. Virtually all pyramidal tract neurons in the motor cortex and area 6 received convergent inputs from the dentate (DN) and the interpositus (IN) nuclei and about 60% of thalamocortical (TC) neurons received convergent inputs from both the DN and the IN. Anterograde labelling following focal injection of Phaseolus vulgaris leukoagglutinin and intracellular staining of TC axons showed that the terminals in layer III tended to aggregate into patches about 1-1.5 mm wide in a frontal plane, which were arranged in longitudinal strips about 2-5 mm long in a rostrocaudal direction.

Afferent Pathways↗
PubMedDate not supplied

Vascular subcortical dementias: clinical aspects.

Vascular dementia (VAD) is common, and small vessel disease is one of the most frequent etiologies of the disorder. Lacunar state and Binswanger's disease are the two types of VAD associated with small vessel disease. Lacunar state and Binswanger's disease produce a dementia syndrome with characteristics of subcortical dementia including slowing of information processing, impaired memory, and poor sustained attention. Executive dysfunction includes poor word list generation and verbal fluency (design generation), impaired motor programming with perseveration and impersistence, and difficulty with set shifting. Memory loss in subcortical VAD is characterized by poor retrieval and intact recognition. Apathy is ubiquitous in VAD and depression and psychosis are common. Parkinsonism with prominent gait disturbances in conjunction with pyramidal tract signs, dysarthria, pseudobulbar affect, and incontinence are frequent motor manifestations of VAD with small vessel disease. The lesions of subcortical VAD affect the structures--caudate nucleus, globus pallidus, thalamus-and connecting fibers of frontal--subcortical circuits and produce a clinical syndrome similar to that seen in other subcortical diseases.

Brain↗
PubMed1989

Neuroepidemiology of human T-lymphotrophic virus type-I-associated tropical spastic paraparesis.

Tropical spastic paraparesis (TSP) is a chronic neurological syndrome of gradual onset involving the pyramidal tracts and upper motor neurons, resulting in weakness and stiffness of the lower extremities, hyperactive tendon reflexes, spasticity, low back pain, and urinary disturbances. Clusters of endemic TSP have been noted in Africa, the Seychelles Islands, Colombia, and the Caribbean. Recently, studies have linked human T-lymphotrophic virus type-I (HTLV-I) with the endemic form of the disease. In Japan a very similar clinical syndrome has been identified as HTLV-I-associated myelopathy and may be a non-tropical version of the same disease. The purpose of the present review is to examine the role HTLV-I may play in the pathogenesis of these myelopathies from a neuroepidemiological point of view.

Adult↗
PubMed1997

Global aphasia-with and without hemiparesis. A linguistic and CT scan study.

The location and size of brain lesions were compared between two groups of patients showing persisting global aphasia according to the criteria of the Aachen Aphasia test (AAT). The first group comprised 8 patients suffering from severe hemiparesis for more than 18 months. The 10 patients of the second group showed either no hemiparesis at all, or motor disturbance at the onset of the disorder with complete remission within 1 year. The sizes of the brain lesions were determined by means of CT scans. The location of the lesions was defined by a statistical model of the brain with labelled anatomical structure, which allowed an interindividual comparison. In the CT scans, the infarcted areas of the brains of patients with hemiparesis always extended to the wall of the lateral ventricle, thus including the whole corona radiata with the pyramidal tract. The infarcted areas of the patients without hemiparesis and with transient hemiparesis spared parts of the deep white matter. The data obtained via CT scans are of prognostic value for patients with transient hemiparesis, since determination of the extent of the lesion by means of CT permits an initial estimate on the possible later degree and quality of the motor recovery.

Aphasia↗
PubMed1980

Adult metachromatic leukodystrophy. III. Clinical course, final stages and first biochemical results.

Continuing the previously published clinical development of a case of adult metachromatic leukodystrophy (MLD), we now describe the terminal phase and death (at 46 years of age) of our patient. The final phase was characterized clinically by progression of generalized peripheral neuropathy, advanced extrapyramidal and pyramidal tract symptomatology, dementia and brainstem dysfunction. First biochemical results show a moderate relative increase (3- to 5-fold) of sulfatides in the frontal lobe white matter but not in the cortex. The analysis of fatty acids in total lipid extract shows a decrease of long-chained fatty acids in favor of short-chained fatty acids, this change is more pronounced in white matter in the cortex. The clinical course and biochemical results are discussed in relation to previous cases analyzed by us. Epidemiological aspects especially emphasize routine serach for MLD amongst patients with neuropsychiatric symptomatology showing unusual psychoses, presenile dementias or unspecific disturbance of motor coordination possibly with electroneurographic evidence of peripheral neuropathy.

Age Factors↗
PubMed1988

Electromyographic and computed tomographic findings in five patients with monomelic spinal muscular atrophy.

Five patients with monomelic spinal muscular atrophy are described. Clinical features included insidious onset of wasting and weakness of one limb, lack of involvement of the cranial nerves, brain stem, pyramidal tracts and sensory system, and a stable condition over a period of 4-20 years. Clinical findings, electromyography and/or muscle biopsy were consistent with anterior horn cell lesion. Central cavities were excluded by magnetic resonance imaging studies of the spinal cord. Computed tomography of skeletal musculature and electromyography indicated more diffuse lower motor neuron involvement by revealing abnormalities in clinically unaffected muscles in 4 of the 5 patients. Myokymic discharges were found in the affected limb of 1 patient.

Adolescent↗
PubMed1992

Magnesium and calcium contents in CNS tissues of amyotrophic lateral sclerosis patients from the Kii peninsula, Japan.

To further elucidate the involvement of metals as a factor in the pathogenesis of amyotrophic lateral sclerosis (ALS) on the Kii peninsula of Japan, a well-known high incidence area of ALS with low calcium and magnesium contents in soil and drinking water, we determined concentrations of these metals in samples of central nervous system tissue taken from postmortem ALS cases. Calcium content was determined by neutron activation analysis and magnesium by inductively coupled argon plasma emission spectrometry. From 5 ALS cases and 5 neurologically normal controls, we examined tissues from the precentral gyrus, including the motor cortex, internal capsule, crus cerebri and spinal cord, and from 22 other areas. The average calcium content in precentral gyrus, internal capsule, crus cerebri and spinal cord in ALS cases was higher than that in the controls, and the mean value of all 26 areas in the ALS cases was also higher than that of the controls. The average magnesium content of each region as well as the mean value of the 26 regions in the ALS cases was significantly lower than that in the controls. The Ca/Mg ratio of the 26 ALS regions was significantly higher than that of controls. This study strengthens our hypothesis that an abnormal metal metabolism plays a responsible role in the Ca-hydroxyapatite formation observed in central nervous system tissue of ALS cases, leading to motor neuron death and degeneration of the pyramidal tracts.

Adult↗
PubMed1994

Predominance of pilocytic histology in dorsally exophytic brain stem tumors.

We report the magnetic resonance imaging (MRI) and clinico-histologic characterization of dorsally exophytic brain stem gliomas (DEBSGs). Between 1983 and 1991, 12 of 51 patients evaluated for the diagnosis of brain stem glioma were found to have DEBSGs emanating from the pons, pontomedullary junction or medulla. Eleven of the 12 patients had classic juvenile pilocytic astrocytomas. Unlike most other brain stem tumors, these patients were young (median 38 months, range 17-75), had a relatively long duration of symptoms (median 7 months, range 2-24) and displayed signs of increased intracranial pressure with limited cranial nerve paresis, absence of pyramidal tract findings, and near normal brain stem auditory-evoked potentials. MRI characteristically showed sharply demarcated lesions with decreased signal intensity on T1, and increased intensity on T2 sequences. Except for cystic areas, these tumors showed bright, uniform enhancement after gadolinium-DTPA. In all patients, 50-100% of the tumor volume could be resected. Three of 10 patients who received no immediate postoperative treatment eventually demonstrated disease progression, and 2 patients with subtotal resections who were treated with radiation and/or chemotherapy postoperatively remain disease-free for extended periods of time. The only death occurred in the 1 patient treated with chemotherapy who died of secondary leukemia. The overall and progression-free survival of these patients at 2 years is 100 and 67% as compared to 18 and 21%, respectively, for other concomitantly treated nonexophytic brain stem gliomas.2+ the ability to achieve significant degrees of resection.

Astrocytoma↗
PubMed1982

Some circuit operations in the mammalian brain.

There is an account of the basis neuronal connectivities of the spinal cord with the Sherringtonian principles of divergence and convergence. Neurones act synaptically either as excitatory or as inhibitory, depending on the specific transmitter substances liberated. Inhibitory neurones usually act either in a feedback or a feedforward manner. Voluntary movement is considered in relation to the instructions delivered to the motor cortex in order to produce the discharges down the pyramidal tract that evoke the required movement. There is an account of the three lines of evidence which indicate that in voluntary movements the primary neural event arises in discharges of neurones of the supplementary motor area (SMA). There are three main circuits from the SMA that activate subroutines concerned in the preprogramming of movements: (1) SMA to the basal ganglia, thence to the thalamus with a collateral line through the substantia nigra, thence to the association cortex; (2) SMA to cerebellar hemisphere via the pontine nuclei, thence to the nucleus dentatus, to the thalamus, to the association cortex, and (3) SMA to association cortex both frontal and parietal. According to the SMA hypothesis the liaison brain for intention is located in the SMA, there being reciprocity of informational flow from the mental events of intention to the neuronal events in the SMA.

Animals↗
PubMed1990

Pontine supranuclear facial palsy.

Two patients presented with a unilateral supranuclear facial palsy. Additional dysarthria was attributed to the pontine origin documented by magnetic resonance imaging on the contralateral side. The pontine disorder also was indicated by an isolated delay of the blink reflex R1 component or of the masseter reflex. We attribute the facial palsy to a lesion of a supranuclear fiber bundle supplying the facial nucleus. The location of the lesions favors these fibers taking a separate course from the main pyramidal tract at the mid- to upper pontine level.

Aged↗
PubMed1995

Syndromes of pontine base infarction. A clinical-radiological correlation study.

BACKGROUND AND PURPOSE: Although there have been sporadic reports of lacunar syndromes due to pontine base infarction, studies of clinical-radiological correlation in sufficient numbers of patients have not yet been reported. METHODS: We studied the clinical features of 37 patients with acute infarcts that mainly involved the base of the pons and correlated the clinical syndromes with the radiological findings. RESULTS: The clinical presentations included pure motor hemiparesis (PMH) in 17, sensorimotor stroke in 3, ataxic hemiparesis (AH) in 4, and dysarthria-clumsy hand (DA-CH) syndrome in 6 patients. Variants of AH included 1 patient with dysarthria-hemiataxia and 2 with quadrataxic hemiparesis, and in 4 patients dysarthria-facial paresis syndrome was considered a variant of DA-CH syndrome. Hypertension was the single most common and important risk factor, and the pathogenetic mechanisms of ischemia were likely to be small arterial (lacunar) occlusion or basilar atheromatous branch occlusion in most of the patients. Our clinical-radiological correlation study suggested that large lesions involving the paramedian caudal or middle pons correlate with severe hemiparesis (PMH), whereas lesions of similar size located in the paramedian rostral pons tended to produce DA-CH syndrome. Lesions producing AH were located variously but tended to spare the pyramidal tracts. The prognosis of these patients is fair or good, although residual hemiparesis remained in patients with initially severe hemiparesis. CONCLUSIONS: Our data suggest that the various lacunar syndromes that follow pontine base infarcts reflect the balance of the involvement of the corticospinal, corticopontocerebellar, and corticobulbar tracts. Analysis of radiological findings aids in determining the clinical-anatomic correlation in patients with pontine base infarction.

Adult↗
PubMed1997

Neurological signs and frontal white matter lesions in vascular parkinsonism. A clinicopathologic study.

BACKGROUND AND PURPOSE: The clinical characteristics and the pathological lesions of so-called vascular parkinsonism (VP) are still debatable. The purpose of this study was to define the core signs and symptoms and assess the cerebrovascular lesions in pathologically confirmed VP. METHODS: In the present study, VP was defined as the presence of parkinsonism and pathological evidence of cerebrovascular lesions but no depigmentation or Lewy bodies at the substantia nigra. We compared the clinical signs and symptoms of 24 VP patients with those of 30 age-matched patients with pathologically confirmed Parkinson's disease. We compared the brain pathology in VP patients with that in 22 age-matched patients with Binswanger's disease (BD) who had no parkinsonism according to clinical records. RESULTS: VP was characterized clinically by a short-stepped or frozen gait, lead-pipe rigidity, absence of resting tremor, and negative response to levodopa. Half or more of VP patients demonstrated pyramidal tract signs and pseudobulbar palsies. There was no significant difference in the extent of vascular lesions at the basal ganglia between patients with VP and with BD without parkinsonism. The extent of frontal white matter pallor tended to be less broad in VP than in BD without parkinsonism. In VP patients, the number of oligodendrocytes in the frontal white matter was significantly less than that in age-matched normal control subjects and significantly more than in those with BD. CONCLUSIONS: The core signs and symptoms of autopsy-proved VP differ from those of typical Parkinson's disease, and most VP patients had diffuse cerebral white matter lesions as well as basal ganglia lesions. VP might be related to frontal white matter lesions.

Aged↗
PubMed1999

High-resolution EEG in poststroke hemiparesis can identify ipsilateral generators during motor tasks.

BACKGROUND AND PURPOSE: Multimodal neuroimaging with positron emission tomography (PET) scanning or functional MRI can detect and display functional reorganization of the brain's motor control in poststroke hemiplegia. We undertook a study to determine whether the new modality of 128-electrode high-resolution EEG, coregistered with MRI, could detect changes in cortical motor control in patients after hemiplegic stroke. METHODS: We recorded movement-related cortical potentials with left and right finger movements in 10 patients with varying degrees of recovery after hemiplegic stroke. All patients were male, and time since stroke varied from 6 to 144 months. All patients were right-handed. There was also a comparison group of 20 normal control subjects. RESULTS: Five of 8 patients with left hemiparesis had evidence of ipsilateral motor control of finger movements. There were only 2 cases of right hemiparesis; in addition, 1 patient had a posteriorly displaced motor potential originating behind a large left frontal infarct (rim). CONCLUSIONS: Reorganization of motor control takes place after stroke and may involve the ipsilateral or contralateral cortex, depending on the site and size of the brain lesion and theoretically, the somatotopic organization of the residual pyramidal tracts. Our results are in good agreement with PET and functional MRI studies in the current literature. High-resolution EEG coregistered with MRI is a noninvasive imaging technique capable of displaying cortical motor reorganization.

Aged↗
PubMed2001

Coherence between cortical and muscular activities after subcortical stroke.

BACKGROUND AND PURPOSE: Functional connection between the motor cortex and muscle can be measured by electroencephalogram-electromyogram (EEG-EMG) coherence. To evaluate the functional connection to muscle between contralateral and ipsilateral motor cortices after pyramidal tract lesions, we investigated 6 patients with chronic subcortical stroke. METHODS: High-resolution EEG and EMG of the hand, forearm, and biceps muscles were recorded during 3 tonic contraction tasks: (1) elbow flexion, (2) wrist extension, and (3) power grip. To evaluate the cortical control of EMG, EEG-EMG coherence was computed. RESULTS: EEG-EMG coherence was localized over the contralateral sensorimotor area in all circumstances, and there was no significant coherence at the ipsilateral side. EEG-EMG coherence was significantly smaller on the affected side for the hand and forearm muscles but not for the biceps muscle. CONCLUSIONS: All direct functional connections to muscle after recovered subcortical stroke come from the contralateral motor cortex. The different effects of the lesion on the proximal and distal muscles appear to be associated with the strength of the corticospinal pathway.

Aged↗
PubMedDate not supplied

Pathology of Minamata disease.

Minamata disease, or methylmercury poisoning, was first discovered in 1956 around Minamata Bay, Kumamoto Prefecture, Japan. A similar epidemic occurred in 1965 along the Agano River, Niigata Prefecture, Japan. The neuropathology of Minamata disease has been well studied; this review focuses on human cases of Minamata disease in Kumamoto Prefecture. Nervous system lesions associated with Minamata disease have a characteristic distribution. In the cerebral cortex, the calcarine cortex was found to be involved in all cases of Minamata disease, particularly along the calcarine fissure. The destruction of nerve tissue was prominent in the anterior portions of the calcarine cortex. Occasionally, the centrifugal route from the visual and visual association areas (internal sagittal stratum) showed secondary degeneration in prolonged cases after acute onset. Postcentral, precentral, and temporal transverse cortices showed similar changes, though they were less severe. Intense lesions in the precentral cortex caused the development of secondary bilateral degeneration of the pyramidal tracts. In the cerebellum, the lesions occurred deeper in the hemisphere. The granule cell population was most affected. In the peripheral nerves, sensory nerves were more affected than motor nerves. Secondary degeneration of Goll's tracts was occasionally seen in prolonged or chronic cases.

Animals↗
PubMed1992

Superficial siderosis of the central nervous system: a neglected cause of sensorineural hearing loss.

Superficial siderosis of the central nervous system is a rare, often unrecognized condition in which there is a deposition of intracellular and extracellular hemosiderin in the leptomeninges, subpial tissue, spinal cord, and cranial nerves as a result of chronic bleeding in the subarachnoid space. On the basis of our cases and a review of the literature, the majority of patients manifest sensorineural hearing loss in addition to cerebellar dysfunction, pyramidal tract signs, and progressive mental deterioration. Recent imaging techniques--particularly CT and MRI--can define the presence of iron deposition, confirming the diagnosis ante mortem. From post mortem specimens, histologic sections demonstrate severe damage to the eighth nerve, with microglial metabolism of iron. Cases will be presented to illustrate these points.

Adult↗