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PubMedDate not supplied

[Paroxysmic anarthria in multiple sclerosis].

INTRODUCTION: The paroxystic clinical features of multiple sclerosis (MS) include trigeminal neuralgia, itch, transient diplopia, Lhermitte's sign, akinesia, dystonia, Uhthoff's phenomenon and others which are very characteristic, such as paroxystic ataxia and dysarthria. CLINICAL CASE: We present the case of a 30 year old man who consulted for multiple episodes lasting only a few seconds, of complete inability to speak. This symptom recurred several times a day and in many different situations. It was often triggered off by external stimuli such as having to speak in front of several people. The disorder disappeared without treatment seven days after onset. Magnetic resonance using fast spin echo image sequences showed multiple hyperintense lesions in mid right cerebellar peduncle, right pons, left temporal lobe, white substance of both internal capsules, periventricular and semioval centres. Biochemical study of the cerebrospinal fluid showed that there were 9 cells/microliter (mainly lymphocytes), proteins 45 mg/dl and a normal glucose level. The Tibling-Link level was 0.73. Cortical somestesic evoked potentials showed slowed conduction after stimulation of the right median nerve and both peroneal nerves. Acoustic evoked potentials of the brain stem were conducted more slowly by the right acoustic pathway at intraxial level. The patient was diagnosed as having clinically defined MS. CONCLUSIONS: We consider that our patient's symptom was a kind of paroxystic dysarthria which we call paroxystic anarthria. Differential diagnosis of this symptom should be basically with phonatory or dysphasic simple partial seizures.

Adult↗
PubMedDate not supplied

[The imaging and electrophysiological correlations in lateral homonymous hemianopsia of vascular origin].

This paper presents 7 cases of patients suffering of lateral homonymous hemianopia. This diagnosis was established taking into account both the clinical exam as well as the visual field, into the context of a vascular suffering of hemiparesis type. I worked with a Bioscript BST 2100 apparatus foreseen with flash and with its help there could have been recorded the visual evoked potentials (VEPs) with electrodes occipitally placed. The analysis of VEPs was made in the correlations with the premises and the extend of the cerebral lesion. The imaging exploration stood out lesions with the following localisations: stretched hemispherically, internal capsule, thalamus, occipitally. The VEPs recordings showed: the small N1 + leveling, the leveling of the whole tract, bifid N1 + leveling, invertit N1 + leveling, diminished N1. The study of the correlation between the lesion premises and the aspect of VEPs led to the idea that waves N1 and P1 represent different functions of the process of the visual stimulations rather than activities in distinct cortical areas.

Aged↗
PubMed2000

[Chronic encapsulated intracerebral hematoma in thalamus with incongruous right homonymous hemianopia: a case report].

We presented a patient with chronic encapsulated intracerebral hematoma. This 49-year-old woman suffered from visual disturbance, and slowly progressive right hemiparesis, sensory disturbance of the right extremities and incongruous right homonymous hemianopia over 2 months. Computed tomography scanning showed high density area and ring enhancement, and magnetic resonance imaging revealed mixed intensity on T1 and T2-weighted images in her left thalamus and internal capsule. Angiographic studies revealed no vascular anomaly or tumor stain. The pathologic pictures indicated well-encapsulated hematoma containing fresh and old hematomas in the left thalamus. Most reported cases of this disease had hematomas in the subcortex and no cases had similar visual disturbance. This report was prepared because this condition is uncommon and may remain unrecognized.

Cerebral Hemorrhage↗
PubMed2000

[A patient with marked immunodeficiency in an HTLV-I carrier: a case report].

We report a 49-year-old man who was an HTLV-I carrier with an immunodeficiency state and intracranial pyramidal tract lesion revealed by MRI. He was born in Hokkaido and was admitted to our hospital because of fluminant hepatitis. On admission, neurologic examination revealed exaggerated deep tendon reflexes including the jaw jerk; the plantar response was flexor. Laboratory examination revealed decrease in the number of lymphocytes and CD4-positive lymphocytes in the peripheral blood and CD4/CD8 ratio was consistently low, indicating the presence of cellular immunodeficiency state. Serum anti-HTLV-I antibody was markedly increased but he did not have HTLV-I associated myelopathy (HAM). He had no underlying disease which would cause immunodeficiency state such as adult T-cell leukemia (ATL) or HIV infection. We concluded that the HTLV-I carrier state induced his immunodeficiency. During the course, he developed retrobulbar neuritis. T2 weighted cranial MRI revealed high signal lesions in the bilateral corona radiata, posterior limb of the internal capsule, and the pontine base, corresponding to the location of the pyramidal tracts. His hospital course was complicated by opportunistic infections such as Pneumocystis carinii pneumonia, cytomegalovirus infections, and meningitis, and died of multiple organ failure 7 months after the admission. Cellular immunodeficiencies in ATL patients are well known. Intracranial central nervous system (CNS) lesions in HAM patients are also mentioned. Recently coincidence of ATL and HAM in the same patients has also been reported. Asymptomatic HTLV-I carriers may have a latent immunodeficiency state and/or CNS lesions. We shall have to be alert about the presence of such carriers.

Carrier State↗
PubMedDate not supplied

[Central pontine myelinolysis and pregnancy: a case report and review of literature].

INTRODUCTION: The 'rapid' correction of hyponatremia, itself a dangerous condition, is dangerous to the patient involved. There is an association between the 'rapid' correction of plasma sodium and the osmotic demyelination syndrome, characterized by the loss of myelin in the pontine neurons, and in extra-pontine sites such as the internal capsule, basal ganglia, cerebellum and cerebrum. Although cases of hyponatremia during pregnancy have been described, it has rarely been possible to demonstrate the condition, by imaging techniques or autopsy, showing demyelination lesions of the cerebrum. We report the case of a pregnant patient who developed this complication and had an interesting response to levodopa. CLINICAL CASE: A 27 year old woman had a history of progressive generalized muscle weakness for the previous six days. She had recently been discharged after receiving treatment for hyperemesis gravidarum. Imaging studies showed pontine and extrapontine myelinolysis. She was treated with levodopa which improved her extrapyramidal symptoms. CONCLUSIONS: Hyponatremia is the most commonly observed electrolyte disorder in the hospital population. The classical symptoms of myelinolysis are spastic quadriparesia and pseudobulbar paralysis, which reflect damage to corticospinal and corticobular paths. Serious symptomatic hyponatremia is a medical emergency which should be managed by specially trained personnel, since the treatment is as dangerous as the condition itself. More investigations are necessary to identify the precise risk factors and the mechanism by which an increase in sodium causes damage to myelin.

Adult↗
PubMed2000

Metastasis-associated mts1 (S100A4) protein in the developing and adult central nervous system.

We have found recently that white matter astrocytes in the spinal cord constitutively express immunoreactivity for Mts1 (S100A4) protein and that this expression is up-regulated ipsilaterally after sciatic nerve or dorsal root injury. Here, we have studied the expression pattern of Mts1 throughout the rat central nervous system (CNS). We found Mts1 immunoreactivity in myelinated tracts such as the olfactory tract, optic nerve, corpus callosum, internal capsule, fimbria, and spinal cord funiculi but not in cerebellar white matter. Mts1-immunoreactive (IR) cells were consistently astrocytic (glial fibrillary acidic protein positive). In addition to myelinated tracts, Mts1 immunoreactivity was also present in a few nonmyelinated or poorly myelinated areas, such as pituitary gland, olfactory bulb, and around the lateral ventricle. Based on location, three Mts1-IR astrocyte groups were distinguished: 1) astrocytes at the surfaces of the CNS, i.e., adjacent to the cerebrospinal fluid, organized perpendicularly to the bundles of axonal tracts; 2) astrocytes located in parallel to, and inserted between, axonal bundles; and 3) clusters of astrocytes around the lateral ventricle and in the olfactory bulb. We further analyzed the relationship between Mts1 immunoreactivity and the development of CNS fiber tracts by combining staining for Mts1 and myelin basic protein (MBP). Mts1 immunoreactivity appeared postnatally in recently myelinated areas. During the development of corpus callosum and the optic tract, Mts1 immunoreactivity was concentrated at the frontier of myelination. The developmental expression pattern suggests a role of Mts1-IR astrocytes in the maturation of myelinated fiber tracts. The preferential localization of Mts1 to the subpial region in the mature CNS suggests that Mts1 participates in astrocyte-mediated CNS-cerebrospinal fluid exchange.

Age Factors↗
PubMed2000

[A 67-year-old man with progressive disturbance of gait].

We report a 67-year-old man with progressive disturbance of gait. He was well until the spring of 1993 (62 years of the age), when he noted an onset of unsteady gait. He also noted that he started to have a difficulty in playing tennis, in which he became unable to hit the ball with his racket. He also noted parkinsonian features such as bradykinesia and loss of hand dexterity. He was treated with levodopa, which did not improve his symptoms. His MRI revealed marked atrophy of the cerebellum and the pons. The criss-cross high signal lesion was seen in the center of the pons. The third ventricle was dilated. The putamen was unremarkable. His subsequent course was complicated by easy to fall, difficulty in swallowing with episodes of aspiration pneumonia. He also developed nocturnal apneustic episodes. He was admitted to our hospital on November 15, 1998, when he was 67 years of the age. He had low grade fever and low blood pressure (98/70). He was anemic but not icteric. Tumors were palpated in his jaw, anterior chest, and in the left arm. He was alert but unable to convey his desire because of dyspnea and tracheostomy. His gaze was slightly restricted in the horizontal direction and markedly so in the vertical direction. Motor functions were difficult to evaluate. His clinical course was complicated by atelectasis of the right lung and pleural effusion. He developed marked edema and oliguria. He developed sudden bradycardia and expired on December 26, 1998. He was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had multiple system atrophy. Majority of the audience agreed with this diagnosis. Post-mortem examination revealed a lung cancer in the right lung (undifferentiated adenocarcinoma) with metastases to the liver, kidneys, lymph nodes, pericardium, pleura, skin, bone marrow, and the brain. Neuropathologic examination revealed marked atrophy of the pons and the cerebellum. The putamen showed brownish discoloration and atrophic changes. The substantia nigra showed marked neuronal loss and gliosis. Oligodendrocytic inclusion bodies (alpha-synuclein positive) were seen in the putamen, globus pallidus, substantia nigra, pontine nucleus, cerebellar white matter, internal capsule, cerebral peduncle, and the spinal cord. These findings are consistent with the pathologic diagnosis of multiple system atrophy. What was interesting to us was the presence of neurofibrillary tangles in the substantia nigra, nucleus ruber, globus pallidus, and subthalamic nucleus. Tuft-shaped astrocytes were also seen. This patient appears to be a rare example of combination of MSA and PSP.

Adenocarcinoma↗
PubMed2000

[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report].

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.

Adolescent↗
PubMedDate not supplied

[Chorea as the presenting form of progressive systemic sclerosis].

We present an exceptional case of a patient with hemichorea of ischemic origin as a form of presentation of progressive systemic sclerosis. The neurologic complications, both central and peripheral, of this condition are considered infrequent and may be due to coexisting or iatrogenic factors, or may be a direct complication of progressive systemic sclerosis. There have been occasional reports of cerebrovascular disease in progressive systemic sclerosis, and this apparent rarity may be related to structural and morphological variations in brain arteries. Recently, there have been reports of primary cerebrovascular changes and vascular calcifications in progressive systemic sclerosis. There are no reported cases associated with movement disorders. The patient is a 66-year-old ex-smoker, and no other vascular risk factors, with chronic Raynaud's phenomenon affecting both hands, and polyarthralgias. Three months previously he began to complain of choreic movements affecting the right-sided limbs without any other neurological manifestations. The abnormal movements responded to haloperidol. There were skin changes suggestive of progressive systemic sclerosis, and capillaroscopy showed abundant avascular zones with dilated capillary loops. Anticentromere antibody titer was elevated to 1/1280. Brain arteriography was normal, and the brain SPECT showed bilateral hypoperfusion bilaterally, predominantly on the left side. Brain MR imaging confirmed an infarct in the left caudate and adjacent internal capsule. The study of this case supports the hypothesis of a direct primary cerebrovascular damage in progressive systemic sclerosis.

Aged↗
PubMed2000

[Encephalomyelopathy demonstrated on MRI in a case of chronic toluene intoxication].

Myelopathy in chronic toluene intoxication is rare. We present obvious lesions of the spinal cord on MRI in a 30-year-old Japanese man with chronic toluene intoxication. He had abused toluene for more than 10 years, and developed visual impairment, horizontal nystagmus, pyramidal tract signs, postural tremor, Romberg's sign, and sensory disturbance below the level of Th 2 dermatome. Anti-HTLV-1 antibody titer and vitamin B12 level in the serum were within normal limits. Biochemical analysis showed no increase of very long chain fatty acids. Cerebrospinal fluid showed no abnormal findings. Auditory brainstem response showed delay of I-V interpeak latency. Somatosensory evoked potential with the median nerve stimulation showed delay of N13-N20 central conduction time, which was later followed by absence of N14-N20 components. On MRI in T2 weighted image, marked high intensity was demonstrated in the posterior limbs of the internal capsule, and in the posterior columns and lateral tracts from the cervical through the upper thoracic cord. Cerebral lesions probably reflect demyelination and axonal degeneration produced by chronic toluene abuse. Spinal cord lesions seem to be secondary to nerve fiber changes more proximal to the nerve cell bodies.

Adult↗
PubMed2000

Putative cortical and thalamic inputs elicit convergent excitation in a population of GABAergic interneurons of the lateral amygdala.

Synaptic circuitry in the rat lateral amygdala (AL) was studied in brain slices using electrophysiological recordings. Electrical stimulation of external and internal capsules evoked an EPSC followed by a sequence of GABA(A) and GABA(B) receptor-mediated IPSC in principal neurons. Paired stimulation of either afferents resulted in a significant reduction ( approximately 45%) of the second GABA(A) receptor-mediated IPSC. A priming stimulation, consisting of a priming pulse to one pathway followed by a pulse to the other pathway, resulted in a strong depression of the second IPSC basically identical to that during paired stimulation. Paired- and primed-pulse depressions were largely relieved by 10 micrometer CGP 55845A, indicating regulation through presynaptic GABA(B) receptors. Furthermore, putative interneurons responded with EPSCs of constant latencies to minimal stimulation of both cortical and thalamic fibers, indicating convergent monosynaptic input. At higher stimulation strength, an approximately 15% reduction of EPSCs occurred in interneurons after paired and primed stimulation, which was not sensitive to CGP 55845A. These findings indicate that a rather homogeneous population of interneurons exists in the AL with respect to their afferent connectivity, in that they receive convergent input through putative thalamic and cortical fibers, both directly and indirectly (through principal neurons), and mediate inhibitory control of postsynaptic principal neurons. This symmetrically built GABAergic circuitry can be of functional significance, given the distinctive role of the two afferent input systems for the mediation of different components of fear responses and the importance of GABAergic mechanisms for limitation of excessive neuronal activity.

Afferent Pathways↗
PubMed2001

Course of motor and associative pallidothalamic projections in monkeys.

As a result of the frequent performance of lesioning and electrical stimulation procedures targeting the globus pallidus internus (GPi) to treat medically intractable hypokinetic and hyperkinetic movement disorders, the course of the pallidothalamic projections originating, in particular, from the motor territory of GPi has important clinical relevancy. To assess the organization of pallidothalamic projections originating from motor and associative portions of GPi, small quantities of the anterograde/ retrograde tracer, biotinylated dextran amine (BDA) were injected into localized regions of the caudal GPi in squirrel monkeys. The localization to motor and associative territories in GPi was confirmed by examining the corresponding regions of retrograde labeling in the striatum and subthalamic nucleus (STN). The labeled pallidothalamic fibers projected principally medially across the inferior edge of the internal capsule. The fiber bundle ventral to the caudal GPi was mainly devoid of labeling. Fibers labeled along the medial and inferior borders of GPi at centrorostral levels were traceable to the medial edge of the injections. The densest fiber labeling at rostral levels was produced by those injections with the greatest extent of rostral labeling of neurons. In opposition to generally accepted schemes, the findings from this study suggest that the pallidothalamic fibers originating from the caudal portions of GPi, including the motor territory, do not course ventromedially to form the ansa lenticularis, but rather, travel predominately medially through the lenticular fasciculus en route to the thalamus. Thus, proposed surgical schemes to target fibers ventral to the caudal GPi or at the rostral pole of GPi appear to be misguided.

Animals↗
PubMed2000

Pathological laughter as heralding manifestation of left middle cerebral artery territory infarct: case report and review of literature.

Clinical, radiological and pathological studies in patients with stroke, presenting with pathological laughter as heralding manifestation, have shown lesions in the internal capsule and thalamus, basal ganglion, hypothalamus and ventral pons. In this report a patient with similar manifestation and having a cortical infarct in the territory supplied by superior division of middle cerebral artery is being presented. Our case suggests possible influence of dominant cerebral hemisphere, especially of Broca's area, on the motor control of laughter.

Dominance, Cerebral↗
PubMed2000

Development and evolution of thalamocortical interactions.

Thalamocortical projections in mammals must travel through a considerable portion of the newly formed subdivisions of the embryonic forebrain. They descend through the ventral thalamus, advance in the internal capsule amongst cells which already possess dorsal thalamic projections, traverse the striatocortical junction, and then reach the cerebral cortex by associating with subplate cells and their early corticofugal fibers. The interactions of the thalamocortical projections with early generated, largely transient cells of these regions are believed to play a crucial role in their deployment. These ideas are supported by recent work on reeler and other strains of mutant mice. While we are beginning to understand the basic pattern of the cellular and molecular interactions employed in mammalian thalamocortical development, comparative developmental studies hold the promise to reveal the underlying logic of these steps and the evolutionary origin of the mammalian cerebral cortex.

Animals↗
PubMed2001

Identification and anatomic description of the anterior choroidal artery by use of 3D-TOF source and 3D-CISS MR imaging.

BACKGROUND AND PURPOSE: The importance of the anterior choroidal artery (AChA) is related to its supply of crucial anatomic structures, such as the internal capsule. Angiographically, the AChA can be detected in 71% to 98% of patients, but as yet, its visibility on MR images has not been evaluated. Our goal was to assess the sensitivity of MR imaging in the identification of the AChA and its anatomic characteristics. METHODS: Twenty volunteers underwent MR imaging with a 3D time-of-flight (3D-TOF) sequence, 10 of them additionally with a 3D Fourier transformation constructive interference in steady state (3D-CISS) sequence. The MR angiographic source images and the 3D-CISS images were analyzed independently by two neuroradiologists, who evaluated the ability to identify the different segments of the AChA and the posterior communicating artery (PComA) according to a previously defined scoring system (0 = not identified, 1 = most probably identified, 2 = identified with certainty). Additionally, three patients were examined who had an arteriovenous malformation (AVM) supplied by the AChA. RESULTS: In the volunteers, the PComA was identified with certainty in 87.5% on 3D-TOF sequences and in 95% on 3D-CISS sequences; the AChA was identified with certainty in 92.5% on 3D-TOF sequences and in 90% on 3D-CISS sequences. 3D-CISS images showed additional anatomic information in six of 20 vessels. In the three patients, the enlarged AChA was identified with certainty on both imaging sequences. CONCLUSION: The AChA can be reliably identified using both 3D-CISS sequences and the source images of the 3D-TOF sequence. MR imaging can be used to assess and follow-up AChA-related disorders, especially AVMs.

Adult↗
PubMed2001

Regional and global changes in cerebral diffusion with normal aging.

BACKGROUND AND PURPOSE: We used quantitative diffusion MR imaging to investigate the microstructural changes that occur in white matter during normal aging in order to identify regional changes in anisotropy and to quantify global microstructural changes by use of whole-brain diffusion histograms. METHODS: Full diffusion tensor MR imaging was performed in 20 healthy volunteers, 20 to 91 years old. Thirteen subjects also underwent high-resolution T1-weighted imaging, so that diffusion images could be coregistered and standardized to normal coordinates for statistical probability mapping. Relative anisotropy (RA) was calculated, as was linear regression of RA with age for each pixel; pixels with a significant correlation coefficient were displayed. For histographic analysis, the average apparent diffusion coefficient (ADC) histograms were calculated on a pixel-by-pixel basis. Subjects were divided into two equal groups by the median age (55 years) of the population and plotted for statistical comparison. RESULTS: Regional analysis showed statistically significant decreases in RA with increasing age in the periventricular white matter, frontal white matter, and genu and splenium of the corpus callosum, despite the absence of signal abnormalities on visual inspection of conventional images. Significant increases in RA were found in the internal capsules bilaterally. ADC histograms showed higher mean ADC and reduced peak height and skew in the older age group on group comparisons. CONCLUSION: Quantitative diffusion histograms correlate with normal aging and may provide a global assessment of normal age-related changes and serve as a standard for comparison with neurodegenerative diseases.

Adult↗
PubMed2001

[Acute disseminated encephalomyelitis in a 3-month-old infant].

Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease showing multifocal central nervous system lesions due to an autoimmune disorder. We reported a 3-month-old girl with ADEM. One week after having a cold, she presented with somnolence, poor feeding and vomiting. When she was admitted three days after the onset, she could neither fix or follow objects with her eyes nor respond to sound. Her muscle tone was decreased. Cerebrospinal fluid examination revealed pleocytosis, elevated protein concentration and positive myelin basic protein. No oligoclonal band was detected. Diffuse monomorphic slow wave activity was noted on the electroencephalogram. Only wave I was present bilaterally on the auditory brainstem response. T2 weighted images of magnetic resonance imaging revealed multiple areas of high signal in the right posterior limb of the internal capsule, white matter of the cerebellum and brainstem. She was diagnosed as having ADEM, and underwent high dose gamma-globulin therapy. Corticosteroids were not given because of her high blood pressure. The clinical symptoms improved continuously before and after the administration. Two years after the onset, she showed normal growth and development without reoccurrence. The age at onset of childhood ADEM is usually 3 or 4 years. ADEM before one year of age is very rare. The demyelinating lesions of this case corresponded to the regions which normally become myelinated by 3 months. Although ADEM is usually treated with corticosteroids, high dose gamma 1-globulin therapy can be considered if patients are very young or have a high risk for corticosteroid, or respond poorly to corticosteroids.

Drug Administration Schedule↗
PubMed1975

Astrocytoma in a dog causing convulsions.

An adult, male, 7 Kg. dog was presented because of a convulsion. This progressed and interictal signs became apparent. A slight left spastic hemiparesis was present with a normal gait and posture. A partial left visual deficit with intact pupillary reflexes became evident. All signs were referable to a right cerebral lesion. Necropsy revealed an astrocytoma in the right cerebrum compressing the internal capsule and optic tract.

Animals↗