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PubMed1998

Acute effects of carbofuran in workers of two pesticide plants.

This paper investigates the acute effects of carbofuran in workers of two pesticide-formulating plants. Mean airborne carbofuran concentrations ranged from 0.025 to 1.115 mg/m3 in plant A and from 0.018 to 0.067 mg/m3 in plant B, respectively. In workers of plant A the post-shift blood cholinesterase activity was significantly reduced, compared to pre-shift values. No difference in blood cholinesterase activity was found between pre- and post-shift values in workers of plant B. During the investigation, 25 cases of acute carbofuran poisoning were diagnosed by their clinical picture and depressed cholinesterase activity in blood. Usual symptoms included dizziness, weakness, blurred vision, nausea and sweating. Pallor, epigastric pain, vomiting and chest tightness occurred only in a few cases. Myosis was recorded in 24 cases. Fasciculation of muscle gastrocnemius induced by percussion was found in 6 cases, and four of them had also fasciculation of muscle orbicularis oculi. Inhibition of cholinesterase activity in the blood was related with the clinical features; however, the inhibition was rapidly reversible. In most cases, recovery was complete within 2-3 hours, with or without atropine treatment, after the subjects were removed from exposure. Rapid onset, mild illness and quick recovery are typical characteristics of occupational acute carbofuran poisoning.

Acute Disease↗

PubMed1999

[An autopsy case with lower motor neuron disease showing a transient-appearance of anti-GM1 antibody and an improvement of conduction block after gamma-globulin administration].

We report a 63-year-old man who died of respiratory failure. He was well until 1992 (57 years of his age), when he had an onset of progressive weakness of the bilateral upper limbs. He showed no improvement with TRH administration in other hospital. On January 12, 1994, he admitted to our department because of the progressive muscle weakness. Neurologic examination revealed a muscular atrophy associated with severe weakness and hyporeflexia in both upper limbs, and fasciculation were seen in his tongue. Electrophysiological studies revealed mild conduction block in the left medial nerve, and F-waves were not evoked in the left ulnar nerve and bilateral median nerves. After an administration of 25 g/day of human gamma-immunoglobulin for 5 days, conduction block as well as F-wave abnormalities in the left median and left ulnar nerve were improved, yet no improvement of muscle weakness was seen. The anti-GM1 IgG titer was transiently elevated in the patient's serum after gamma-immunoglobulin therapy. On September 8, 1994, subtotal gastrectomy was performed because of the early stage gastric cancer. Histological examination showed poorly differentiated adenocarcinoma (signet-ring cell carcinoma). His muscle weakness had been gradually extended to the lower limbs and he couldn't walk himself on January, 1998. On March, 1998, he developed tetraplegia, mild dysphagia, dysuria and the respiratory disturbance. On April 12, 1998, he admitted to our department for the second time. Neurologic examination revealed a muscular atrophy and fasciculation associated with severe weakness in all of his limbs, tongue and musclus masseter. Neither deep tendon reflex nor pathologic reflex was evoked in his upper and lower extremities. His ocular movements and sensations were well preserved. He died of respiratory failure on May 1, 1998. The patient was presented in a neurological CPC. Neurological and laboratory findings suggested a spinal progressive muscular atrophy (SPMA). However, there were several unusual points as a typical SPMA in this case, that is, an improvement of the electrophysiological abnormalities by gamma-globulin treatment, as well as transient elevation of anti-GM1 antibody. The clinical neurologists have arrived at the conclusion that the patient had lower motor neuron syndrome associated with anti-ganglioside antibody and cause of death was ascribed to the respiratory failure. We discussed whether this case was SPMA or multifocal motor neuropathy. Postmortem examination revealed numerous diverticulums in the ascending colon and lymphothyroiditis. No recurrent carcinoma was detected. Neuropathologically, both severe atrophy of the anterior spinal roots, and severe gliosis and neuronal loss in the anterior horn of the spinal cord were observed. Onuf nuclei were not affected. Neurogenic muscular atrophy was detected in the tongue, diaphragm, and limb muscles. Motor neurons of the brainstem were relatively preserved, but skein-like inclusions as detected by anti-ubiquitin antibody, were present in the facial and hypoglossal nuclei. Neither motor cortex nor cortico-spinal tracts were affected. Demyelination, remyelination or cellular infiltrations were not apparent in the right median nerve and sciatic nerves. The neuropathologic features were compatible with SPMA.

Autoantibodies↗

PubMed2000

The dendritic architecture of the cholinergic plexus in the rabbit retina: selective labeling by glycine accumulation in the presence of sarcosine.

The cholinergic amacrine cells in the rabbit retina slowly accumulate glycine to very high levels when the tissue is incubated with excess sarcosine (methylglycine), even though these cells do not normally contain elevated levels of glycine and do not express high-affinity glycine transporters. Because the sarcosine also depletes the endogenous glycine in the glycine-containing amacrine cells and bipolar cells, the cholinergic amacrine cells can be selectively labeled by glycine immunocytochemistry under these conditions. Incubation experiments indicated that the effect of sarcosine on the cholinergic amacrine cells is indirect: sarcosine raises the extracellular concentration of glycine by blocking its re-uptake by the glycinergic amacrine cells, and the excess glycine is probably taken-up by an unidentified low-affinity transporter on the cholinergic amacrine cells. Neurobiotin injection of the On-Off direction-selective (DS) ganglion cells in sarcosine-incubated rabbit retina was combined with glycine immunocytochemistry to examine the dendritic relationships between the DS ganglion cells and the cholinergic amacrine cells. These double-labeled preparations showed that the dendrites of the DS ganglion cells closely follow the fasciculated dendrites of the cholinergic amacrine cells. Each ganglion cell dendrite located within the cholinergic strata is associated with a cholinergic fascicle and, conversely, there are few cholinergic fascicles that do not contain at least one dendrite from an On-Off DS cell. It is not known how the dendritic co-fasciculation develops, but the cholinergic dendritic plexus may provide the initial scaffold, because the dendrites of the On-Off DS cells commonly run along the outside of the cholinergic fascicles.

Animals↗

PubMed2000

Early postnatal expression of L1 by retinal fibers in the optic tract and synaptic targets of the Syrian hamster.

Previous immunohistochemical studies in mouse, rat, and chick have reported that the expression of the glycoprotein and cell adhesion molecule L1, a member of the immunoglobulin superfamily, shows regulation during development of retina and optic nerve. To extend our understanding of the role of L1 in developing neural circuitry, we have examined L1 expression in the optic tract and thalamic and midbrain synaptic targets of retinal fibers in the early postnatal Syrian hamster, a well-characterized developmental model of the primary visual projection. Metabolic labeling studies reveal that a synaptically targeted, sulfated, and glycosylated form of L1 undergoes rapid axonal transport from the retina. Retinofugal transport of L1 decreases commensurate with the decline in immunoreactivity of retinal fibers in the visual pathway. Retinal ganglion cell axons show intense L1 immunoreactivity as they navigate in highly fasciculated bundles in the optic tract overlying the lateral geniculate body and in the superior colliculus. We found no evidence of L1 immunoreactivity on retinal axon collaterals as they defasciculate from the optic tract and branch into target neuropils. L1 immunoreactivity wanes in optic tract as axon terminal arbors are elaborated in the lateral geniculate body and superior colliculus and as myelination in the visual pathway commences. This pattern of L1 expression suggests that, in the early postnatal period, L1 may support fasciculation of retinal fibers, maintaining them within the optic tract, and that subsequent down-regulation of L1 may facilitate their terminal arborization and myelination.

Age Factors↗

PubMedDate not supplied

[Hypernephroma associated motor neuron disease. Presentation of a case].

INTRODUCTION: Paraneoplastic motor neuron disease are rare among patients with renal cell carcinoma. OBJECTIVE: Present the clinical and electrophysiological evolution of a patient with a motor neuron disease and hypernephrome. CASE REPORT: A 60 years old woman, affected only by high level pressure since 10 years ago. She noticed sudden palsy of the left leg and 10 months later an abdominal ultrasound showed a renal cell carcinoma, discovered without other symptoms than neurologic. After radical nephrectnomy, the patient was treated with recombinant interferon alpha 2b. The neurologic damage advanced and she has a flaccid weakness and muscle atrophy in the legs and brisk reflexes, also in wasted limbs. There is Babinski, fasciculations, light flaccid dysarthria and laryngospasm. Peripheral nerve conduction studies are within normal limits. The electromyogram show positive sharp waves in both legs and left hand. Recruitment patterns are decreased and there are fasciculations in the tongue, upper and lower limbs. The magnetic resonance of the brain and spinal cord is normal. There are not evidence of metastasis. The question of whether or not this is a paraneoplastic form of motor neuron disease remain unclear. CONCLUSION: This case suggest the need to consider a renal cell carcinoma in the course of a motor neuron disease.

Carcinoma, Renal Cell↗

PubMed1992

[A clinicopathological study on 13 cases of motor neuron disease with dementia].

Thirteen patients suffering from motor neuron disease with dementia were studied to analyze the clinicopathological spectrum. The diagnosis of the disease was made on the basis of a clinical history of progressive dementia and motor neuron involvement. The mean age at onset of 11 sporadic cases was 54.9 years (range, 43 to 69 years), with a mean duration of disease of 25 months (range, 11 to 47 months). The initial symptoms were dementia in 7 cases, motor neuron involvement in 2 cases, and both dementia and motor neuron involvement in 2 cases. The clinical picture of motor neuron disturbance in sporadic cases represented bulbar-type of amyotrophic lateral sclerosis (ALS). Bulbar palsy was the initial symptom in 7 sporadic cases and all 11 patients developed bulbar palsy with advancing course of illness. Muscular wasting and fasciculation were more predominant in the upper limbs, shoulder girdle and anterior chest. Fasciculation was more extensively and frequently observed in those portions than that of classical ALS. In contrast, muscle strength in the lower limbs was well preserved so that all patients could walk even when respiratory failure developed. Hyperreflexia including jaw jerk was found in all cases and positive Babinski sign in 7 cases. Parkinsonism appeared in the initial stage in one sporadic case and in two familial cases. The type of dementia with uninhibited behavior and personality change closely mimicked that of Pick's disease. The degree of dementia was mild or moderate in 8 cases and severe in 3 cases. Language disorder was characterized by progressive reduction of speech output, leading finally to mutism in 5 cases. Perseveration was observed in 10 cases. Visuospatial disorder was absent even in the advanced stage. Mild memory disturbance was noted in the early stage in 10 cases. Pathological examination was performed in 7 cases including one familial case, revealing frontal atrophy in 3 cases, frontotemporal atrophy in 2 cases and temporal atrophy in 2 cases. On microscopic examination there were mild neuronal loss, gliosis, mild spongy state of the cortical superficial layers and fibrous gliosis in the frontotemporal white matter. The scattered senile plaques in one case did not justify a diagnosis of Alzheimer's type dementia. Neither circumscribed atrophy nor Pick body was found in any case. The nucleus basalis of Meynert showed no neuronal loss. The substantia nigra showed a mild to severe loss of nerve cells without Lewy bodies in all cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed2003

The morphological and functional basis of the new conception about the suprarenal cortex regeneration.

The exhaustion of main intracellular and cellular reserves of the regeneration in suprarenal cortex under the influence of exogenous hyperthermia activates the supplementary sources of cellular regeneration. First type of low differentiated cortical cells appears under the outer connective tissue capsule on approximately the 7(th) day of hyperthermia. These cells proliferate and some of them migrate along the cortical blood capillaries towards the deep portion of zona fasciculate. They differentiate into the typical cortical cells (spongiocytes) of zona glomerulosa and zona fasciculate according to their location. Second type of low differentiated cortical cells appears through one circadian-septal period (during 7 days) near the inner connective tissue capsule that separate cortex from the medulla. This cell type gradually differentiates into the typical cortical cells of zona reticularis. Stem cortical cells were found in suprarenal cortex. They did not have specific morphological signs and could synthesize nucleus DNA.

Adrenal Cortex↗

PubMed2004

Brachial plexopathy: a clinical and electrophysiological study.

BACKGROUND: A retrospective study to evaluate the clinical and electrophysiological profile of brachial plexus lesions in a tertiary care center of India. METHODS: Thirty eight patients with brachial plexopathy (idiopathic or traumatic) with detailed electrophysiological studies were sampled. This included detailed motor and sensory nerve conduction studies of the conventional median, ulnar and radial nerves of the upper limbs, CMAP from deltoid, biceps and triceps on stimulating the ERB's point, needle EMG in the appropriate muscles and paraspinal muscles. The electrophysiological studies were performed on both sides irrespective of the clinical involvement and were recorded within 1.61 +/- 2.89 months in idiopathic group and 2.11 +/- 2.65 months in traumatic plexopathy group. The severity of involvement was assessed on MRC scale. ADL scale was used to assess the disability at presentation and subsequent follow up. RESULTS: 12 patients (11 male and 01 female) had idiopathic brachial plexopathy and 26 patients (all male) had traumatic brachial plexopathy. In the idiopathic group the lesion was localized to upper trunk in 58.3% of patients and middle trunk (posterior cord) in 41.66% and none had lower trunk or diffuse involvement. 25% had bilateral involvement. Two patients (16.6%) with idiopathic plexitis had recurrence involving the opposite side during the follow up. In the traumatic group the lesion was localized to the upper trunk in 11.53%, middle trunk (posterior cord) in 57.69% and 30.76% of patients had diffuse involvement. All the patients in traumatic plexopathy group had severe disability while in idiopathic group 91.66% had severe disability and 8.33% had moderate disability. Low amplitude CMAP and F wave abnormality were seen in 16.6% of patients in idiopathic group. On needle EMG 83.3% had fasciculation or fibrillations while none had paraspinal EMG abnormality. In traumatic group low to absent CMAP was seen in 69.2% and 76.92% had F wave abnormality. SNAPs were not recordable in 53.8%. On Needle EMG all the patients showed fasciculation or fibrillations and only 6 (23.0%) had paraspinal muscle fibrillations. Root avulsion could be documented in only four of these cases on MR imaging. CONCLUSIONS: Recovery in the traumatic group correlated well with the electrophysiological abnormalities while no such correlation was evident in the idiopathic group.

Adolescent↗

PubMed2004

Electrodiagnostic evaluation of motor neuron disorders.

Amyotrophic lateral sclerosis (ALS) is the most common adult motor neuron disorder and leads usually to death within two to five years after diagnosis. Clinically, ALS presents with fasciculations, progressive weakness, muscle atrophy, and spasticity. It is a clinical diagnosis, supported by electrodiagnostic and laboratory tests. Nerve conduction studies (NCS) and needle electromyography (EMG) are essential in the evaluation of suspected ALS. NCS are primarily used to exclude any potentially treatable motor neuropathy that may mimic ALS. Standard nerve conduction studies should include at least four sensory and four motor nerves in an arm and leg. At least three sites in three different nerves should be stimulated when searching for conduction blocks, which may distinguish motor neuropathy from ALS. Needle EMG is very valuable as it can demonstrate widespread involvement of muscles that are not clinically weak. Characteristic findings include widespread non-myotomal denervation (both acute and chronic), with fibrillations and fasciculations. Extensive needle examination should include at least two limbs (arm and leg; at least five muscles each), thoracic paraspinal and bulbar muscles.

Amyotrophic Lateral Sclerosis↗

PubMedDate not supplied

[Nogo-A functions during the development of the central nervous system and in the adult].

OBJECTIVE: The myelin-associated inhibitors play a very important role in preventing the regeneration of the adult central nervous system. Among these inhibitors it is Nogo-A, a recently cloned protein expressed by oligodendrocytes. However, after its discovery as a myelin-associated protein, there has been described new functions for Nogo-A far from its role in the oligodendrocytes myelin. DEVELOPMENT: After an introduction to the molecular changes that occur after a central nervous system (CNS) injury we focus in the figure of Nogo-A and its family of proteins. Finally, we make a revision of the different functions that have been described to date for Nogo-A, from the development of the CNS to the inhibition of axonal regeneration in the adult, highlighting the therapeutic potential of the selective blockade of Nogo-A. CONCLUSIONS: Although Nogo-A was discovered in the context of axonal growth inhibition, in which it is indeed playing a determining role, Nogo-A has turned out to be also a neuronal protein involved in diverse processes that go from axonal fasciculation to apoptosis. As we deepened in our knowledge about the molecular mechanisms that organize the complex functioning of the CNS, it is clearer that the proteins implicated in fasciculation and axonal guidance during development also play equally important roles in mechanisms like the axonal inhibition or the regulation of the synaptic plasticity in the adult CNS.

Adult↗

PubMed1992

Neurite growth on different substrates: permissive versus instructive influences and the role of adhesive strength.

Growing axons use environmental cues to guide them to their targets. One class of cues is thought to be adhesion molecules on cells and in the extracellular matrix that axons interact with as they grow to their targets. In choosing between two possible pathways, the relative adhesiveness of the two substrates could be an important factor in controlling neurite growth. We conducted experiments in vitro to study how naturally occurring adhesion molecules influence neurite growth. Neurite growth rates, the degree of neurite fasciculation, the choices neurites make between two substrates, and the relative adhesiveness of different substrates were examined. We found that the relative adhesiveness of a substrate was a poor predictor of either axon growth rate or the degree of fasciculation. Furthermore, neurites showed little selectivity between three different naturally occurring substrates, L1, N-cadherin, and laminin. These results suggest that some adhesion molecules may serve as permissive substrates in that they can define axonal pathways but they do not provide information about which path to take at a choice point or about which direction to go along the path. Finally, these results suggest that substrates in vivo may not exert their effects on axon guidance principally via relative adhesiveness.

Adhesiveness↗

PubMed2004

[A case of dementia with motor neuron disease associated with agraphia--the omission of kana letters].

We report a 55-year-old right-handed Japanese man with motor neuron disease and dysgraphia of kana letters. He was admitted to our hospital because of dysarthria and dysphasia. On admission, the results of general physical examination were within normal limits. Neurological examination revealed severe dysarthria, dysphasia, impaired movement of the tongue without fasciculation and slight distal muscle weakness in the bilateral upper limbs. There were no fasciculation of the muscle. Deep tendon reflexes were hyperactive without Babinski's signs. Sensation, coordination, and gait were normal. Neurophysiological studies demonstrated normal motor nerve conduction velocities and sensory action potential. The results of needle electromyography of the upper limbs were compatible with motor neuron disease (MND). Magnetic resonance imaging (MRI) showed atrophy of the bilateral temporal region of the brain. 99mTc-HMPAO SPECT (Single Photon Emission Computed Tomography) showed reduced uptake of tracer in the bilateral temporal region. On neuropsychological examination, his behavior was normal, and orientation and intelligence were also preserved, but his speech was severely impaired. Reading comprehension was slightly impaired. In regard to writing comprehension, he had no difficulty in copying of words though dictation was found to be impaired. He omitted one kana letter in a word. Agraphia is accompanied by various factors such as aphasia, dementia, agnosia, alexia. But in this case at least for early stage, agraphia existed without other higher cortical dysfunction. He did not show severe dementia in his early stage of his disease, but developed it later in the disease's progression. In this case, agraphia might be due to the atrophic changes in the temporal lobe.

Agraphia↗

PubMed2005

[Morpho-functional alterations of the adrenal cortex in rats with active and passive strategy of adaptive behavior].

In rats with the active (KHA strain) and passive (KLA strain) coping strategies, a post-stress depression develops respectfully on the 1st or 10th day after the inescapable stress. The present study revealed an increase of adrenal weight and blood corticosterone levels on a day following the inescapable stress, as well as marked fluctuations of blood glucose in one and five days post-stress in KHA rats. By the 10th day, these indices returned their basal levels. In contrast, the stress reactivity of KLA rats was lower in all terms and their corticosterone levels remained reduced on the 10th day after stress. In KLA rats, the fasciculate zone was reduced but reticulated zone grew in Ith day following the stress, while in KHA rats the inescapable stress resulted in growth fasciculate zone and concomitant reduction of reticulate zone, both evident on the 10th post-stress day. The data indicate that the development of post-stress depression in KLA rats is probably associated with exhaustion of adrenocortical function.

Adaptation, Psychological↗

PubMed2004

The virtue of being too early: Paul A. Weiss and 'axonal transport'.

The essay introduces how Paul A. Weiss (1898-1989) analyzed his data on neuronal outgrowth and axonal transport, supported by constriction experiments of thousands of living mature nerve fibers. At the University of Chicago his group measured the steady proximo-distal flow of nerve fibers. To visualize the data he used tissue culturing, light microscopy, radioactive tracers, time-lapse motion pictures and electronmicroscopy. The work resulted in the discovery of fasciculation of outgrowing nerves and a computation of the rate of axonal transport, published in a classical article in 1948. He stated that the outgrowth of nerve fibers occurs from nerve centers in their nucleated cell bodies by fasciculation and protein synthesis. However, at that time one suspected the published microphotograph to be an idealized image and, therefore, did not accept the analysis, or the 'new' knowledge. In the mid 1960s the improved technique of autoradiography confirmed in an indirect way Weiss data and analysis of axonal transport. The objective here is to show (1) how Weiss employed the visibility of micrographs and drawings to corroborate his observations and analysis on axonal dynamics, and (2) to offer some tentative suggestions why his colleagues did not accept the 'neuro-images' as an evidence of new knowledge.

Axonal Transport↗

PubMed1991

Clinical and electrophysiological assessments in ALS patients.

Since the relationships between traditional assessments in ALS patients have not been defined, three clinical and four electrophysiological assessments were performed in a cross-sectional study of 87 ALS patients. The clinical assessments produced Norris ALS scores, muscle strength scores and illness durations (DUR). The electrophysiological assessments produced scores for motor unit interference pattern, denervation potentials, compound muscle action potential, and fasciculations. The individual muscle scores were averaged to produce mean scores, and Spearman rank correlations were performed on the mean scores. The association between Norris ALS and mean muscle strength (MMS) scores is significant (p less than .001, rs = 0.84), and these scores are significantly correlated with mean interference pattern (0.77, 0.82), mean denervation potential (-0.63, -0.70), and mean compound muscle action potential scores (0.55, 0.60), respectively. Correlations between IP and DP scores (-0.71), IP and CMAP scores (0.62), and DP and CMAP (-0.56) scores are also significant. Scatterplots of the data and regression lines suggest linear relationships between each of these assessments. Illness duration and fasciculation scores are not strongly correlated (rs less than 0.55) with any of the other clinical or electrophysiological assessments.

Amyotrophic Lateral Sclerosis↗

PubMed1991

[A case of Kennedy-Alter-Sung syndrome with type IIa hyperlipidemia--study on sex hormone receptor and lipid metabolism].

A 57-year-old man of Kennedy-Alter-Sung syndrome (K-A-S) with type IIa hyperlipidemia was reported with studies of several sex hormone receptors. He noticed tremulous movements of hands on gripping at age 40 and gynecomastia at age 46. He had been pointed out to waddle since 52 years old, and also noticed difficulty in going up stairs and standing up at age 54. He was admitted to our Neurology Service on June 5, 1989. On general physical examinations, gynecomastia, eyelids xanthomas and hypertrophy of Achilles tendons were found. Neurologic examination revealed clear consciousness and slight dysarthric speech with nasal voice. Cranial nerves showed mild bilateral facial weakness, poor uvula and soft palatal movements, atrophy and weakness of bilateral sternocleidomastoid muscles, and atrophy of tongue with fasciculation. The four extremities were hypotonic, and proximal muscular atrophy and weakness of four extremities were seen. Deep tendon reflexes were absent in four extremities and fasciculation on both thighs was noted on contraction. Sensory and cerebellar functions were intact. Waddling gait and Gowers' sign were present. In K-A-S syndrome, abnormal lipid metabolism such as a family of type IIa hyperlipidemia, or familial and sporadic cases of type IV hyperlipidemia has been documented. In the family of our cases, his elder sister was found to have type IIa hyperlipidemia, while his son had type IV hyperlipidemia. The coexistence of these two types of hyperlipidemia in the same family of K-A-S syndrome has not been reported so far to our knowledge.(ABSTRACT TRUNCATED AT 250 WORDS)

Achilles Tendon↗

PubMed1991

Motor neurone disease in Thailand: the clinical aspects of 77 patients.

This is the first large scale case series of motor neurone disease (MND) in Thailand. Seventy-seven patients were identified between 1978 and 1984 at Siriraj Hospital Medical School, Bangkok, Thailand. Fifty-five patients were male (71.43%) and the mean age of the patients was 51.55 (SD 14.26) years with the range of 17 to 78 years. Clinical classification of MND was categorized as progressive bulbar palsy (PBP), 26 patients (33.77%); amyotrophic lateral sclerosis (ALS), 42 patients (54.54%); and progressive spinal atrophy (PSA), 9 patients (11.69%). The mean age of PBP, ALS and PSA were in the order of 57.61 (SD 12.09), 52.81 (SD 11.18), and 28.11 (SD 9.44) years. Progressive spinal atrophy group was younger than PBP and ALS groups significantly at the P-value less than 0.05 by analysis of variance and Duncan tests. Fifty-three patients (72.60%) were resident in Bangkok and the central part of Thailand. The main presenting symptoms were wasting of the small muscles of both hands, leg weakness, and speech and/or swallowing difficulties. These symptoms were found in 62 patients (81.58%). Nearly half of the patients (48.68%) came to our care within six months of onset, 22.8 per cent presented with asymmetry of motor wasting, while limb and trunk fasciculation was seen in 73.61 per cent. Dysarthria, dysphagia and tongue fasciculation were recorded as 51.32, 48.68, 60.53 per cent respectively. Exaggerated deep tendon reflexes were noted as 65.79 and 80.26 per cent over the upper and lower limbs, while Babinski sign was elicited in only 23.3 per cent of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Restless legs syndrome associated with diminished cardiopulmonary compliance and lumbar spinal stenosis--a motor concomitant of "Vesper's curse".

Lumbosacral and associated leg pain and paresthesias arousing patients from a sound sleep, or Vesper's curse, has been previously reported. An increase in right atrial filling pressure reflected in elevated paraspinal venous volumes within the reduced confines of a stenotic lumbar spine has been cited as the cause of this syndrome. Six cases of concomitant nocturnal calf cramps and fasciculations associated with the night pain and paresthesias are reported. In all cases a reduction in cardiopulmonary compliance was noted, with clinical and electromyographic evidence of paraspinal and lower extremity fasciculations increasing at night. Symptoms were relieved by assuming an erect or semi-reclining sleep position. In five of the six reported cases of lumbar spinal stenosis, spondylolisthesis was also present. The motor equivalent of Vesper's curse was evaluated by electromography, evoked potentials, CAT scan, and myelography. The multiple factors involved in the pathomechanics and pathophysiology of lumbar radiculopathy, and spinal stenosis and the role of the paravertebral plexus of veins are reviewed as they relate to the genesis of the restless legs syndrome.

Aged↗