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PubMed1990

[Effects of enkephalins on associative processes of parietal cortex neurons].

Experiments on cats examined the effect of met- and leu-enkephalins on the process of learning of the parietal associative cortex neurons (field 5). It has been shown that conditioned electrical stimulation of the pyramidal tract axons with nociceptive reinforcement evoked plastic changes of responses in 35 neurons. It was found that the effect of microiontophoretically applied enkephalins on these neurons depend on the time of iontophoretic application. When endogenous opioid peptides were applied up to 30-40 min they inhibited the process of elaboration of temporary connection.

Animals↗
PubMedDate not supplied

[Folate and the nervous system (author's transl)].

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.

Anticonvulsants↗
PubMedDate not supplied

Human immunodeficiency virus within the brains of children with AIDS.

Infants and children with symptomatic human immunodeficiency virus (HIV) infection frequently develop neurologic disease with symptoms and signs of acquired microcephaly, developmental delays, encephalopathy, pyramidal tract signs, and less often, movement disorders and ataxia. However, clinical courses vary and, based upon progression of neurologic findings, we have classified them into 2 broad categories; progressive (loss of previously acquired language and cognitive skills) and plateau (failure to acquire additional developmental skills). We have used immunocytochemistry to localize HIV within the brains of neurologically involved children with AIDS. Interestingly, the brains of those children with a progressive neurologic course showed readily detectable HIV antigen, while those with a plateau course showed little or no detectable HIV. These findings suggest that in children with symptomatic HIV infection, the progressive neurologic deterioration is due to continued presence of HIV within deep white matter and gray matter, while the plateau neurologic course is due to HIV induced damage followed by either limited penetration of virus into the central nervous system, or clearance of virus below detectable limits.

AIDS Dementia Complex↗
PubMedDate not supplied

Enterovirus diseases with neurological determinations in adults. Clinical and virological study.

Enteroviruses--4 polio, 30 Coxsackie and 20 echovirus strains--were isolated from 54 patients with neurologic disease. In 29 cases (53.7%) viruses were isolated from the CSF, blood clot and nerve tissue homogenates. The correlation of the complex clinical data and the localisation of the lesions in the CNS demonstrate the involvement of cranial nerves, of the long bulbar motor pyramidal and extra-pyramidal tracts, of the reticular formation, a.o. These aspects are in accordance with the localisation of the lesions especially in the brain stem and in the hypothalamus, in most of our patients. The extent and complexity of the lesions suggest a predominatly vascular dissemination.

Adult↗
PubMed1990

Periodic leg movements during either epidural or spinal anesthesia in an elderly man without sleep-related (nocturnal) myoclonus.

We report a case of periodic leg movements (PLM) observed in an 86-year-old man during either midthoracic epidural anesthesia or spinal anesthesia. The PLM observed were stereotyped (extension of the big toe in combination with partial flexion of the ankle, knee, and hip lasting 3-5 s) and repetitive (interevent intervals between jerks were 20-40 s) for about 120 and 30 min respectively. The patient was awake but unaware of the PLM unless reminded. The present case was quite similar to sleep-related (noctural) myoclonus (SRM) in every respect except for its occurrence during wakefulness. SRM is more prevalent in the elderly population but its mechanism remains to be elucidated. Previously, we had reported a case of PLM observed in an elderly man with SRM. In our two cases, PLM were seen only while the local anesthetic was acting on the spinal cord; therefore, these anesthesia-related PLM (ARPLM) may suggest that the spinal cord is involved. In particular, we consider that physiological changes seen commonly during non-rapid-eye-movement sleep and a certain phase of anesthesia, such as suppression of the descending inhibitory pathway, and pyramidal tract dysfunction are relevant to ARPLM. In addition, the concomitant alteration of the blood flow in the leg and changes due to aging of the spinal cord may also be involved.

Aged↗
PubMed1990

[A case of Binswanger disease with numerous diffuse plaques in the neocortex].

A case of Binswanger disease with numerous diffuse plaques in the neocortex was reported. This male patient had a previous history of hypertension and myocardial infarction. From the age of 60, he developed dysarthria, bradykinesia, marche à petit pas and falling down. Neurological examination at his first admission disclosed muscular rigidity and increased jaw and deep tendon reflexes, but dementia was not found. Brain CT showed moderate brain atrophy and EEG consisted of slow wave dysrhythmia. He was diagnosed of Parkinsonism and treatment started without effects. During his second admission for the treatment of myocardial infarction, at the age of 64, delirium developed. Progressive dementia began and finally he was confined to bed. From the age of 69, spontaneous speech became almost lost. Contracture of the extremities, increased deep tendon reflexes and force grasping were noted. Brain CT showed symmetrical low attenuation in the frontal and parietal white matter with moderate dilatation of the lateral ventricles. At the age of 70, he died of general prostration about ten years after the initial symptoms. Neuropathological findings: Macroscopic findings: The brain weighed 1300 g. Atherosclerotic changes of the large arteries at the base of the brain were moderate. Coronal sections of the brain showed moderate enlargement of the lateral ventricles with multiple small lacunes in the basal ganglia. Microscopic findings: Bilateral diffuse demyelination of the white matter with sparing of the U-fibers was noted. Holzer stain revealed fibrillary gliosis in the left parietal and occipital white matter. Marked adventitial fibrosis of the deep white matter arteries and terminal stages of hyalinosis of the perforating arteries were found. Basal ganglia showed status lacunaris. Bilateral pyramidal tracts were atrophic secondly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Amplitude and latency characteristics of spinal cord motor-evoked potentials in dogs.

The motor-evoked potential can be reliably recorded in anesthetized dogs by use of percutaneous placement of active recording electrodes near the dorsal lamina of the vertebral column. Two types of responses were observed in this study; short (less than 5.5 ms at T9-10)- and long (greater than 5.8 ms at T9-10)-latency waves. Short-latency waves are larger in amplitude and appear with higher stimulus intensities than do long-latency waves. Short-latency waves are conducted at greater than 80 m/s and may not reflect pyramidal tract activation. The safety of using higher intensity stimuli to generate short-latency waves has not been determined.

Animals↗
PubMed1990

[The restructuring of the efferent activity of the generator of scratching during the electrical activation of the descending systems].

Rearrangement of the scratching generator activity evoked by phasic electrical stimulation of different descending systems has been investigated on decerebrated immobilized cats. This rearrangement heavily depends on the stimulation phase. Maximal increase of the scratching cycle duration by electrical stimulation of Deiters' nucleus, red nucleus and pyramidal tract takes place in the first half of an aiming phase. The electrical stimulation of structures mentioned above does not practically change duration of the scratching cycle in the second half of the aiming phase and at the beginning of the scratching phase. A maximal increase of the scratching cycle duration by electrical stimulation of reticular gigantocellular nucleus occurs in the second half of the aiming phase. The electrical activation of descending pathways during the aiming phase increases intensity of this phase and decreases intensity of the scratching phase. The electrical activation of descending pathways during the scratching phase increases its intensity and does not change practically the intensity of the aiming phase. Possible principles of the suprasegmental correction of the scratching generator activity are discussed.

Animals↗
PubMed1990

[Central motor conduction time (CMCT) in hereditary motor sensory neuropathy type I (HMSN type I)].

The motor system of 13 cases with hereditary motor sensory neuropathy (HMSN) type I were analysed by clinical neurophysiological method. The motor conduction velocity (MCV) and F wave latency in lower motor neurone were markedly delayed. The latency of the muscle evoked potential (MEP) by cortical magnetic stimulation were also markedly delayed. The central motor conduction times (CMCT) were calculated by two methods. CMCT-mag was calculated by subtraction of the MEP by cervical magnetic stimulation from the MEP by cortical magnetic stimulation. CMCT-f was calculated by subtraction of the [(F wave latency -1 + distal latency)/2] from the MEP by cortical magnetic stimulation. There were positive correlation between CMCT-f and CMCT-mag. CMCT of HMSN type I were divided to two groups. CMCT of the first group was markedly delayed. CMCT of the second group was mildly delayed or normal. The former group showed marked weakness in distal muscles clinically. The latter group showed mild or moderate weakness in distal muscles clinically. All these patients did not show any pyramidal tract signs, which could be covered by severe lower motor neurone involvements. The classification of HMSN type I by gene was well known, genetical analysis might be important to these groups in HMSN type I.

Adolescent↗
PubMed1989

[Centrifugal influence from the cortical taste area on neural activity of the parabrachial nucleus in rats].

To reveal the functional significance of fiber connections from the cortical taste area (CTA) to the parabrachial nucleus (PBN), a combined study with neuroanatomical and electrophysiological techniques were performed on male Wistar rats anesthetized with urethane. The results were as follows: 1. Tracing of WGA-HRP showed that the fibers connecting the CTA and PBN passed through the central tegmental field (CTF). 2. Injection of glutamate into the PBN and electrical stimulation of the PBN elicited copious salivary secretion. Electrolytic lesion of the CTF and ibotenic acid lesion of PBN neurons diminished salivary secretion induced by electrical stimulation of the CTA. These results suggest that some PBN neurons receive inputs from the CTA and send axons to the lower brain stem for salivary secretion. 3. Electrical stimulation of the CTA induced both salivary secretion and jaw movements. Lesions of the CTF at the inferior colliculus level inhibited the cortically induced salivary secretion, but did not affect the jaw movements. On the contrary, lesions of the pyramidal tract (PT) at the same level inhibited jaw movements, but did not affect salivary secretion. These results suggest that corticofugal fibers concerned with salivary secretion pass through the CTF and those concerned with jaw movements pass through the PT. 4. Of 61 PBN neurons that responded to taste stimuli, 14 (23%) showed facilitatory (F), 11 (18%) facilitatory-inhibitory (F-I), 1 (2%) inhibitory-facilitatory (I-F), and 2 (3%) inhibitory (I) responses to single pulse stimulation of the ipsilateral CTA. Repetitive CTA stimulation induced F responses in 16 (33%) and I responses in 6 (12%). This proportion of F and I responses was essentially the same in any groups of neurons classified by responsiveness to taste stimuli.

Animals↗
PubMedDate not supplied

MR Imaging of the cervical cord in juvenile amyotrophy of distal upper extremity.

We report the MR studies of the cervical cord in seven patients presenting juvenile muscular atrophy of distal upper extremity. This illness, also known as monomelic amyotrophy or benign focal amyotrophy, is distinct from the other motor neuron diseases. Seen in young males, it is characterized by muscular atrophy of the hand, and usually of the forearm, most often unilateral. The underlying process, of unknown origin, affects the anterior horn cells in the lower cervical cord. The gradual onset of purely motor disturbances may mimic early amyotrophic lateral sclerosis. This latter diagnosis may be excluded because of clinical stabilization and lack of pyramidal tract involvement. In our series, five MR studies were positive. In three cases we were able to demonstrate focal and unilateral atrophy in the lower cervical cord limited to the anterior horn region. Morphologic MR findings correlated with clinical and electromyographic features. In two other cases the MR-clinical correlation was more complex. No pathologic MR signal was detected on either T1- or T2-weighted images. Although the diagnosis of monomelic muscular atrophy is based on neurologic and neurophysiologic data, MR provides confirmatory evidence as well as useful information contributing to an understanding of this disease.

Adolescent↗
PubMed1989

[A case of meningoencephalitis caused by persistent Epstein-Barr (E-B) virus infection].

A 44-year-old man had several episodes of tingling sensation in his lower extremities, head and face over 1 year and presented mental disturbance 2 months prior to admission. He additionally suffered from dysuria and acute onset of gait disturbance 18 days before admission. Physical and neurological examination revealed marked splenomegaly, stupor, abnormal behavior, spastic tetraparesis and sphincter disturbances, and meningoencephalitis was suspected. There was lymphocytosis in peripheral blood, some of which showed atypical morphology. CSF examination revealed increased protein content and mononuclear pleocytosis. The titers of antibodies against E-B virus were elevated as follows; VCA IgM (X320), VCA IgG (X20,480), EA (X10,240) and EBNA (X10) in serum, and VCA IgM (X4), VCA IgG (X160), EA (X40) and EBNA (less than 1) in CSF. CT and MRI examination revealed ring enhanced lesion adjacent to left lateral ventricle with surrounding diffuse edema. Administration of intravenous glycerol and oral prednisolone induced substantial improvement in sensory, mental and sphincter disturbances and brain CT findings but not in splenomegaly and pyramidal tract signs. Antibody titer against VCA IgM also decreased. After withdrawal of prednisolone, CSF and CT findings worsened, and the antibody titer became elevated again, and CSF and CT findings improved by readministration of prednisolone. From the above signs and laboratory data, especially continuous elevation of antibody titer against E-B VCA IgM for as long as 1 year, this case was considered to be a meningoencephalitis caused by persistent E-B virus infection.

Adult↗
PubMed1989

Encephalopathy as a presentation of pediatric AIDS: case report.

Fifty to ninety percent of pediatric AIDS cases are complicated by neurologic dysfunction. We present a case of a 5-year-old black female with AIDS encephalopathy and Mycobacterium avium intracellulare. Her initial presentation was that of neuroencephalopathy with loss of developmental milestones, pyramidal tract signs, and subsequent evidence of cortical atrophy. Her initial CT scan at the time of frank encephalopathy was normal, whereas 18 months into the clinical course of her encephalopathy, her CT scan of the head demonstrated typical ventricular dilatation and severe cortical atrophy consonant with her clinical picture. She subsequently developed Mycobacterium avium intracellulare documented by gastric aspirate culture and other opportunistic infections including Candida esophagitis. Her neuroencephalopathy plateaued with continued evidence of immune dysfunction and mycobacterium by gastric aspirate, despite triple antibiotic therapy with INH, streptomycin, Pyrazinamide with later addition of Rifampin and final substitution of the investigational congener Rifabutin. AIDS encephalopathy and Mycobacterium intracellulare are discussed in terms of their prognosis and therapy, particularly in view of new reports of the application of AZT and immunoglobulin therapy.

AIDS Dementia Complex↗
PubMed1989

[Intracytoplasmic eosinophilic inclusions in dorsal root ganglia and spinal nerve roots from an autopsy case of unusual familial ataxia with cerebrospinal fluid abnormality].

Studies were performed on the light and electron microscopic structures of the dorsal root ganglia (DRG) and spinal nerve roots of the 4th lumbar nerve obtained by autopsy from a 49-year-old man with unusual familial ataxia, who showed varied neurological manifestations such as progressive ataxia, action tremors, pyramidal tract signs, mild deep sensory disturbances and autonomic dysfunctions during a 30-year period of illness, and had 2 siblings, one male and female, similarly affected and close consanguineous marriages in his family. On laboratory examinations, blood chemistry disclosed no significant findings. Repeated spinal taps showed constant xanthochromia and elevated protein in the cerebrospinal fluids. A PEG and cranial CTs revealed a progressive brain atrophy. NCVs and EMGs in the extremities were within normal limits. There was no chromosomal abnormality. Light microscopically, intracytoplasmic eosinophilic inclusions (IEIs) with pale rim, which showed varied sizes and rounded shapes, occurred within neurons in the DRG, particularly in small neurons. Many of the small neurons had numerous IEIs, and several rounded granules with a high degree of eosinophilia, measuring below 5 microns in diameter. Generally the small neurons showed atrophic, while most large neurons showed no remarkable change although they had a small number of IEIs and granules located in the perikaryal periphery. Most satellite cells, and some Schwann cells in the DRG, ventral and dorsal roots had IEIs similar to those seen in the neurons. No IEIs occurred intraaxonally, and there was seen no degenerative process in the DRG and roots except a connective tissue fiber proliferation in the DRG.(ABSTRACT TRUNCATED AT 250 WORDS)

Ataxia↗
PubMed1989

[A nosological study of a patient showing ataxia & lower motor neuron involvement].

A sporadic case of spinocerebellar degeneration with prominent involvement of the motor system has recently been encountered. A 54-year-old man without family history noticed speech disturbance at the age of 46 and weakness in his right hand the following year. The muscle weakness and atrophy were slowly progressive and made walk impossible at the age of 50, when his dysphagia increased. At the age of 54, he was admitted to our hospital when neurological findings revealed marked amyotrophy of general skeletal muscle and tongue with fasciculation. Deep tendon reflexes were decreased. Cerebellar ataxia was impossible to evaluate because of profound muscle weakness. And sensory disturbance was suspected in the distal portion of the lower extremities. CT scan revealed progressive atrophy of the brain stem and cerebellum. The patient died at the age of 54 due to CO2 narcosis. The clinical course was 8 years. A summary of the pathological findings was as follows: 1) Marked neuronal loss of the anterior horn of the spinal cord and motor cranial nerve nuclei except for oculomotor nuclei, with mild degeneration of pyramidal tract below lumbosacral level. 2) Degeneration of cerebellipetal system, spinocerebellar tract, Clarke's column and the middle root zone and cerebellifugal system, dentate nucleus, superior cerebellar peduncles, and red nucleus. 3) Mild degeneration of pontine nuclei, inferior olivary nuclei, pontine transverse fibers, the middle and inferior cerebellar peduncles, cerebellar white matter and Purkinje cells as in OPCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyotrophic Lateral Sclerosis↗
PubMed1989

[In vivo inspection of Wallerian degeneration. MRI studies].

11 cases of infarction with Wallerian Degeneration studied by Magnetic Resonance Imaging. It showed that MR Imaging is a very useful method to inspect Wallerian degeneration in vivo after cerebral infarction and provides a new way to study neural pathways. T2-Weighted Images can demonstrate the degenerated pyramid tract and the extent of the degeneration. T1-Weighted Images can demonstrate structural changes clearly such as the atrophy of the cerebral peduncle.

Aged↗
PubMed1989

[Palilalia associated with progressive supranuclear palsy].

Two cases of progressive supranuclear palsy (PSP) with palilalia were presented. Case 1: A 64-year-old woman was in good health until age 62 when she noted clumsiness in walking. Subsequently, forgetfulness, abrupt falls and difficulty in swallowing developed. At the age of 63, she tended to repeat same words in conversation. On admission, neurological examination revealed mental deterioration (Hasegawa's scale 19), unsteady emotional state, supranuclear vertical gaze palsy, pseudobulbar palsy, nuchal dystonia, pyramidal tract signs and extrapyramidal signs. Although spontaneous speech production was reduced, she could answer to questions with compulsive repetition of a phrase or word. She always repeated twice or three times without stuttering, logoclonus or "palilalie aphone". Case 2: A 68-year-old, right-handed woman noted double vision since about one year ago. Subsequently, she developed slowness of voluntary movement, forgetfulness and difficulty in walking. Neurological examination showed similar signs as Case 1. She was not palilaic on examination, however we found the description of her palilalia on nurse's working records. Palilalia was not present so constantly as Case 1, but continued for about a year. We suppose that palilalia is not a rare phenomenon in PSP. Although the pathogenesis of palilalia is unknown at present, we speculate the combination of extrapyramidal sign, pseudobulbar palsy and dementia may most contribute the pathogenesis of palilalia on PSP.

Aged↗
PubMed1989

Atlantoaxial subluxation and hydrocephalus [corrected] in rheumatoid arthritis.

We report a case of rheumatoid arthritis with anterior and vertical atlantoaxial subluxation. Our patient developed severe spastic quadriparesis and pyramidal tract signs. Cephalic computerized tomogram scan showed evidence of evolutive communicating hydrocephalus and the odontoid peg protruding in the posterior fossa. The patient recovered after cerebral spinal fluid ventricle-peritoneal shunting and occipitocervical arthrodesis. No other neurologic complications occurred during a 6-year followup.

Arthritis, Rheumatoid↗