Leg Paralysis Research Articles

Acute paraplegia: A presenting manifestation of aortic dissection

Two patients who presented with acute paralysis of the lower extremities as an initial manifestation of aortic dissection are described. The first patient had transient chest pain followed by flaccid paralysis of her lower extremities and severe back pain. In the second patient, sudden paralysis of both legs developed without pain of any sort. The paraplegia completely resolved in a few minutes; however, chest and back pain later ensued. Both patients had a proximal (type I or A) aortic dissection. The first patient's entrance tear in the aortic intima was just above the aortic valve with antegrade propagation, whereas in the second patient, the entrance tear was at the aortic isthmus, with both antegrade and retrograde dissection. Acute cardiac tamponade resulted in sudden deterioration and death in both patients, before any therapeutic intervention could be entertained.

Paralysis and lameness associated with aflatoxicosis in broilers

Two cases of aflatoxicosis in broilers were characterised, unusually, by trembling, ataxia, paralysis of legs and wings and lameness. Histopathology showed severe degeneration of hepatocytes, bile duct proliferation and depletion of lymphocytes in the lymphoid organs. Aspergillus flavus was isolated from the feed and litter. Aflatoxin B1 was detected in one sample at a concentration of 2.4 mg/kg.

Research Note: Effects of Dietary Butylated Hydroxyanisole and Cysteine on Toxicity of Lathyrus odoratus to Broiler and Japanese Quail Chicks

The effect of .75% dietary butylated hydroxyanisole (BHA) and 1% cysteine on the toxicity of Lathyrus odoratus seed to Japanese quail and broiler chicks was examined. In both species, the feeding of Lathyrus seed as a component of a complete diet depressed (P<.05) body weight gain and feed intake. Typical signs of lathyrism, including ruffled feathers, enlarged hocks, curled toes, ataxia, leg paralysis, and mortality, were observed. Neither BHA nor cysteine exerted protective effects against the lathyrogenic effects. As assessed by mortality, these additives appeared instead to potentiate Lathyrus toxicity.

腰神経根引き抜き損傷の一例

Traumatic lumbosacral nerve root avulsion has been recognized as extremely rare, compared with traction injury of cervical lesion. This seems to due chiefly to the structural characteristics of the mechanism of lumbar girdle. But recently, with the development of high speed transport, so called high momentum injury has been increasing.We report a case of a 58-year-old woman who sufferred from right 4th lumbar nerve root avulsion in the traffic accident.She had fractures of right pelvic ring and right transverse process of the 5th lumbar spine.Mechanism of this injury seemed to be left side bending of lumbar spine and fiexion-abduction displacement of right thigh.In treating a case of pelvic fractures associated with flaccid paralysis of lower leg, we must take into consideration an avulsion injury of the lumbar nerve root.

Peripheral neuropathy associated with dietary riboflavin deficiency in the chicken. I. Light microscopic study.

Chickens fed a riboflavin-deficient diet from hatching had leg weakness and paralysis as early as 12 days of age. Signs worsened through day 16; after 35 days, recovery was evident. Sciatic nerves from affected chickens were enlarged. Significant microscopic lesions were confined to peripheral nerves and included tissue separation (suggesting interstitial edema), Schwann cell swelling, perivascular leukocytic infiltration, and segmental demyelination accompanied by accumulation of osmiophilic debris in Schwann cell cytoplasm. Axon degeneration was present, but was not a primary lesion. Acid phosphatase enzyme activity of Schwann cells was increased in affected nerves. These results demonstrate that dietary riboflavin deficiency causes a demyelinating peripheral neuropathy in young, rapidly growing chickens.

Viral strain dependent differences in experimental Argentine hemorrhagic fever (Junin virus) infection of guinea pigs.

Guinea pigs infected with low-passage Junin virus of human origin showed viral strain dependent differences in mortality, LD50, time to death, and in viral spread and distribution. Different Junin strains appeared to cause at least two broad patterns of Argentine hemorrhagic fever in guinea pigs. A number of strains of Junin virus caused a viscerotropic type of illness in which virus replicated predominantly in lymph nodes, spleen, and bone marrow. With the most severe visceral forms of Argentine hemorrhagic fever, the guinea pigs became viremic, developed necrosis of spleen, lymph nodes, and bone marrow, showed gastric hemorrhages, and all animals died within 13-15 days. Other Junin strains induced a neurological type of illness with transient viral replication in and lymphocyte depletion of spleen and lymph nodes, with no detectable viremia or viral replication in bone marrow. Subsequently, virus was found in the brain with varying severities of polioencephalitis, and the guinea pigs frequently showed rear leg paralysis before death occurred 28-34 days after inoculation. Not all animals infected with a neurotropic strain developed all these signs. One viral strain induced some signs characteristic of both patterns of illness. Although the disease forms in the guinea pig model did not strictly correlate with those observed in the humans from which these strains were obtained, the different strains of Junin virus consistently caused very different patterns of illness in infected guinea pigs.

Extra-anatomical bypass formation and exclusion of thoracic aortic aneurysms by "paired clamp method": the development of hind leg paralysis, the thrombus formation and the pressure ratio between the excluded cavity and the aorta.

The extra-anatomical bypass formation and the exclusion of thoracic aortic aneurysms by the "paired clamp method" applied to the thoracic aorta of mongrel dogs, and the development of hind leg paralysis was studied experimentally in relation to the ratio between the mean excluded cavity pressure and the mean aortic pressure ratio (EA-ratio). The relationship between thrombus formation in the excluded cavity and the EA-ratio was also studied. Animals were divided into 4 groups: Group 1 underwent the cross-clamping of the descending thoracic aorta for 8 min; Group 2 underwent exclusion of the entire thoracic aorta under permanent bypass; Group 3 underwent ligation of 2/3 of the proximal intercostal arteries which branched from the excluded thoracic aorta; and Group 4 underwent division of the excluded thoracic aorta into 3 parts by ligation. No animals in group 1 developed paralysis. When EA-ratios were higher than 0.48, animals in groups 2 and 3 were not paralyzed, whereas all but 1 animals with EA-ratios lower than or equal to 0.48 were paralyzed. There was statistically significant difference between the EA-ratio of the non-paralyzed animals and that of the paralyzed animals in groups 2 and 3. Four out of 5 animals in group 4 were paralyzed. However, there was no statistically significant difference between the EA-ratio in these 4 paralyzed animals and that in the non-paralyzed animals in groups 2 and 3. When the EA-ratio was lower than or equal to 0.59, all but 1 excluded cavities of groups 2 and 3 animals were fully thrombosed 7 or 8 days after the operation. None of these animals showed the aggravation of the paralysis during the observation period and, conversely, the paralysis of almost all animals was ameliorated. These results suggested that the EA-ratio is useful in predicting the development of paralysis and thrombus formation in the excluded cavity after the operation of thoracic aortic aneurysms by the "paired clamp method".

常染色体優性遺伝を示したＣｈａｒｃｏｔ‐Ｍａｒｉｅ‐Ｔｏｏｔｈ病の一家系例

Charcot-Marie-Tooth disease, which was reported separately by Charcot, Marie and Tooth in 1886, is also called progressive neural muscular atrophy or peroneal muscular atrophy.This disease is considered to develop usually in patients over 20 years of age, beginning with paralysis of legs, especially common fibular nerve-supplied region, and then progressing slowly in the central direction, but with good vital prognosis. It is also indicated well for orthopedic functional reconstructive operation because of its paralysis involving only legs below knee joints.This time, we experienced a genealogical case of such disease presenting autosomal dominant inheritance, and reported here the results of its examination.

Studies on the distribution of lidocaine in tissue after spinal and intravenous application in rabbits: clinical and forensic toxicological aspects.

Distribution of lidocaine in tissue was investigated after spinal anesthesia and intravenous application in rabbits to examine aspects of forensic and clinical toxicology. Respiratory arrest occurred at 5-15 min after injection of 5 mg/kg hyper-baric lidocaine solution into the subarachnoid space followed by standing in the head down position. The minimum concentration of lidocaine in the middle part of the cervical spinal cord of the dead rabbits was 197 micrograms/g. On the other hand, maximum concentration in the same site at the critical state of almost complete respiratory arrest was 175 micrograms/g. The time at which the concentration of lidocaine reached a maximum in plasma and various tissues after subarachnoid administration was 10-15 min. The concentrations in the lumbar spinal cord, a site of administration, were 1200-1500 micrograms/g 5 min after the injection, which decreased gradually to about 180-250 micrograms/g at 60 min when paralysis of the hind legs began to recover. According to these data, the concentration of lidocaine in the spinal cord of rabbits required for neural blockade was presumed to be about 200 micrograms/g. Since the maximum concentrations of lidocaine in each tissue was already observed at 2.5 min after intravenous injection, transport of lidocaine from plasma to tissues was considered to be very rapid. Lidocaine accumulates most rapidly in the spleen and kidney, followed by the brain, lung, heart, spinal cord and plasma. The concentration in the liver was the least because of its hepatic metabolism. Distribution to adipose tissue was slower than that to other tissues, but the highest accumulation was observed at the late stage. Elimination rates of plasma and tissues other than adipose were almost the same.

Incompatibility between lasalocid and chloramphenicol in broiler chicks after a long-term simultaneous administration.

Two growth experiments were conducted to evaluate in broiler chicks the compatibility between lasalocid medication in the feed (at 90 or 125 ppm) and a long-term administration of chloramphenicol either via the feed (500 ppm) or via the drinking water (500 mg/liter). The simultaneous administration of lasalocid and chloramphenicol generally caused severe growth depression, decreased feed intake and impaired feed conversion. Several chicks showed evident symptoms of intoxication, such as ataxia, leg weakness and paralysis. The development and frequency of these symptoms were dependent on the dosage of lasalocid and on the duration of the simultaneous administration. Biochemical examinations (Experiment 2) revealed in the affected chicks significant changes in several parameters, in particular a markedly increased activity of creatine kinase and GOT in the plasma. It confirmed that the observed leg weakness and paralysis were caused by myodegeneration.

Experimental allergic encephalomyelitis (EAE): Role of B cell and T cell epitopes in the development of EAE in lewis rats

Studies from our laboratory have shown that classical clinical and histological signs of experimental allergic encephalomyelitis (EAE) may be induced in Lewis rats by synthetic peptides S49 or S55. Peptides S49S and S55S are defined by residues 69-84 and 72-84 of the guinea pig myelin basic protein (MBP), respectively. Peptide S53 (residues 75-84 of the guinea pig MBP), six residues shorter than S49S at the N-terminal end, induced mild clinical signs of disease unaccompanied by hind leg paralysis, incontinence, or central nervous system pathology. In contrast, peptide S67 (residues 69-81 of the guinea pig MBP), three residues shorter than S49S at the C-terminal end, did not induce either clinical or histological signs of EAE despite the fact that the S67-sequence houses an epitope known to induce cell-mediated immunity. Peptides S49S, S55S, and S53 are antigenic and gave rise to antibodies that recognized either of the three peptide sequences. In this report we explore the interrelationship between cellular immunity induced by the S67 sequence and humoral immunity, induced by the S53 sequence and the development of classical clinical and histological signs of EAE. The results show that the nonencephalitogenic sequence of S67 may be rendered encephalitogenic in the presence of antibody directed against the S53 sequence. Lewis rats immunized with S53 developed pathological signs of EAE only after they were challenged with S67. The fact that a simultaneous challenge with S67 and S53 was as effective in inducing EAE pathology as a delayed one (up to 40 days) suggests that the cellular response to S67 is dependent upon the humoral response to S53.(ABSTRACT TRUNCATED AT 250 WORDS)

DM-20, a proteolipid apoprotein, is an encephalitogen of acute and relapsing autoimmune encephalomyelitis in mice.

Experimental allergic encephalomyelitis (EAE) was successfully induced in BALB/c mice with DM-20, a protein component of proteolipid apoprotein. DM-20 was separated by ion exchange column chromatography with CM-Trisacryl from proteolipid apoprotein obtained from bovine spinal cords. Its purity was ascertained by SDS-polyacrylamide gel electrophoresis, a dot immunobinding procedure, and amino acid analysis. Nine of 15 animals with a single injection of 100 micrograms of DM-20 and five of seven animals with a booster injection developed hind leg paralysis or axial rotatory movement 16 to 27 days after sensitization (mean 21.3 days). Five of the 14 animals relapsed 2 to 6 wk after the first attack. Histological examination revealed inflammatory lesion, with significant demyelination in the central nervous system. Antibody levels to DM-20 were not related to the clinical signs. Five of 11 BALB/c nude mice reconstituted with T cells developed similar clinical and pathologic signs. This DM-20-induced EAE in mice may provide a valuable model because it is similar to multiple sclerosis and because it can be induced in inbred mice in which immune mechanisms can be easily studied.

Ross river virus mutant with a deletion in the E2 gene: Properties of the virion, virus-specific macromolecule synthesis, and attenuation of virulence for mice

A mutant of RRV T48 the prototype strain of Ross River virus has been isolated with a 21-nucleotide deletion in the gene coding for the envelope glycoprotein E2. Direct sequencing of the 26 S subgenomic RNA, together with HaeIII and TaqI restriction digest analysis of cDNA to RNAs from cells infected with the mutant virus (RRV dE2) and with RRV T48, were consistent with the deletion being the only major alteration in the mutant genome. The E2 protein of RRV dE2 virions had a higher electrophoretic mobility than that of RRV T48 E2 protein. Neither RRV dE2 nor RRV T48 virions contained more than trace amounts of E3, the small envelope glycoprotein found in Semliki Forest virus. RRV dE2 generated small plaques on Vero cell monolayers; plaque formation was not temperature-sensitive between 32 and 41°. By comparison with RRV T48 the infectivity of RRV dE2 virions was thermolabile at 50°. In BHK cells RRV dE2 grew with similar kinetics to RRV T48. Rates of synthesis of 26 S RNA and 49 S RNA were higher in cells infected with RRV dE2 than in cells infected with RRV T48. Virus-specific protein synthesis and shut-down of host protein synthesis occurred 2–3 hr earlier in RRV dE2-infected cells than in cells infected with RRV T48. Minor differences between the two viruses were observed in the profiles of virus-specific proteins generated in infected cells. In day-old mice RRV dE2 induced less severe symptoms of hind leg paralysis than did RRV T48. A small increase in LD 50 and average survival time was observed in RRV dE2-infected mice by comparison with RRV T48 infected mice. Peak titers reached by RRV dE2 in the hind leg muscle, brain, and blood of day-old mice were 3–4 log units less than the titers reached during infection with RRV T48. In week-old mice the differences in virulence between the two strains were magnified: RRV dE2 induced no detectable symptoms even when injected at high doses (8 × 10 6 PFU) whereas the LD 50 and average survival time for RRV T48 were unchanged from those in day-old mice. Peak RRV dE2 titers in hind leg muscle, brain, and blood, respectively, were 2, 5, and 5 log units less than the corresponding titers for RRV T48. Peak muscle titers reached by RRV dE2 were similar (∼10 8 PFU/g tissue) in day-old mice where lethality was high and in week-old mice where the virus was avirulent. In brain tissue, peak RRV dE2 titers were 10 7 and 10° PFU/g, respectively, in day-old and week-old mice. Since the corresponding figures for RRV T48 were 10 11 and 10 9 PFU/g, the outcome of RRV infection was probably determined more by the extent of replication in neural tissues than in muscle tissues.

RECOVERY AND CHARACTERIZATION OF TEMPERATURE-SENSITIVE MUTATIONS AFFECTING ADULT VIABILITY IN DROSOPHILA MELANOGASTER

Temperature-sensitive (ts) autonomous cell-lethal mutations have been used extensively to study important developmental phenomena, such as pattern formation, in Drosophila. Their utility would be enhanced considerably if it were possible to establish which cell type is primarily affected by each lesion. To facilitate such an approach we have isolated and characterized 21 EMS- induced X-linked adult-lethal (adl) mutants, 16 of which are ts. Most of these lesions also elicit ts lethal effects during preimaginal development. They represent 19 different loci distributed randomly along the X chromosome. The general properties of these mutations are described. In addition, results of an in-depth analysis (focus mapping and, in some cases, temperature shift and heat-pulse studies) of four strains, adl-1(ts) (1), sesE, adl-2(ts) ( 1) and rex are reported. Two major temperature-sensitive periods (TSPs) of adl-1 lethality were resolved: one during the second half of embryogenesis and the other coinciding with pupariation. Mosaic analysis revealed separate mesodermal foci for leg paralysis. Developmental analysis of adl-1 embryos suggest that the adl-1 product may be required for maintenance of muscle tissue. Two discrete TSPs of sesE lethality exist: one during the second instar and the other extending from late third instar to early pupation. Mosaic analysis of sesE lethality resolved a pair of neural foci, each of which appears to incorporate three separate foci for leg paralysis. Mosaic analysis of adl-2(ts) ( 1) revealed the existence of paired lethal foci that appear to map to the vicinity of the subesophageal ganglion. Analysis of rex mosaics resolved separate mesodermal foci for leg paralysis.

Neurologic complications in oral polio vaccine recipients

Between April 1982 and June 1983 four children 3 to 24 months of age were referred for evaluation of neurologic abnormalities found to be compatible with vaccine-related poliovirus infection, which had not been suspected by referring physicians. Patients were epidemiologically unrelated residents of Indiana, and none had prior symptoms suggestive of immunodeficiency. All had received poliovirus vaccine orally (first dose in three, fourth dose in one) and a diphtheria-tetanus-pertussis injection in the left anterior thigh within 30 days of symptoms. A vaccine-like strain of poliovirus was isolated from each patient, and each had symptoms (left leg paralysis in three; developmental regression, spasticity, and progressive fatal cerebral atrophy in one) persisting for at least 6 months. Immune function was normal in two with poliovirus type 3 infection, and abnormal (hypogammaglobulinemia, combined immunodeficiency) in two with type 1 and type 2 infection, respectively. The incidence of observed vaccine-related poliovirus infection in Indiana recipients of orally administered poliovirus vaccine was 0.058 per 100,000 per year, significantly greater (P less than 0.001) than predicted.

Delayed neurotoxicity in the wild mallard duckling caused by the organophosphorus insecticides cyanofenphos and leptophos

The susceptibility of wild mallard ducklings to the delayed neurotoxic effect of the neurotoxic organophosphorus insecticides cyanofenphos and leptophos was evaluated following a daily dosing regimen. Ducklings were treated daily with either cyanofenphos or with leptophos at different dose levels for 90 days, or until they died, or became paralyzed. A control group of ducklings given corn oil at 1 ml/kg daily for 90 days was used for comparison. All treated birds were observed daily for any clinical signs of neurotoxicity during the course of this study. All of the surviving ducklings that were treated with cyanofenphos at 4 mg/kg/day or leptophos at 10 mg/kg/day developed clinical signs of delayed neurotoxicity after 7 to 11 weeks of intoxication. Symptoms included leg weakness, ataxia, severe ataxia and paralysis. The observed clinical signs were confirmed by histological changes found in the spinal cords of the treated birds. These changes were of the type associated with organophosphorus-induced delayed neuropathy (OPIDN). These results demonstrate that wild mallard ducklings are susceptible to OPIDN and this avian species can be used in screening organophosphorus compounds for such effect.

Morphological changes of neurons in experimental avian encephalomyelitis.

Cerebrospinal lesions of chicks experimentally infected with avian encephalomyelitis (AE) virus were investigated morphologically. Central chromatolysis in motor neurons was mostly reversible, while affected Purkinje's cells revealed necrosis with glial reaction. Direct fluorescent antibody technique revealed various amounts of granular antigen in Purkinje's cells of all chicks showing marked leg paralysis. AE virus particles, 25nm in diameter, were found in crystalline arays in the cytoplasm of the same cells.

Skeletal muscle aging in the hind limb of the old male Wistar rat: inhibitory effect of hypophysectomy and food restriction

By age 1 100 days (37 mth) hind leg paralysis was found in 50% of ad libitum fed (control) male Wistar rats, but only 10% of food restricted rats and no hypophysectomized rats of that age had this disease. Gastrocnemius-muscle weight declined at a faster rate than whole body weight in old ad libitum fed rats but not in old hypophysectomized or food restricted rats. Light microscopic and ultrastructural changes were studied in the muscles of the hind limbs of 11 control, 5 food-restricted and 5 hypophysectomized rats aged 805 to 1307 days. Light microscopic changes in muscles involved progressive degeneration demonstrated by the accumulation of adipocytes and degenerative inclusion bodies. The main ultrastructural changes were associated with myofibrillar breakdown. In addition there was thickening of the basal lamina around blood capillaries. However, muscle from hypophysectomized and food restricted rats of the same age range as controls possessed normal morphology with reduced thickening of the capillary basal lamina.

Studies on the toxicity of some carbamate fungicides in Drosophila melanogaster meig. (insecta, diptera)

This paper reports the effects of three commercial powders mixed into the diet, Dithane M-45 (mancozeb 80%), Pomarsol (thiram 80%) and Peltar (maneb 50% and methyltiophanate 25%) on survivorship of adults Drosophila and on the progeny. With wild-type adults (Oregon), fungicides were added to the diet at the rate recommended on the label. The mean lifespan was reduced by 42.5% (Pomarsol), 50% (Dithane M-45), and 83% (Peltar). For larvae of two strains (Oregon and triploid) intoxicated with Dithane M-45 and Peltar, a linear relationship was demonstrated between the doses and the percentage of the progeny reduction. The calculated doses inducing a 50% reduced progeny (PR50) are in the range of 400 to 700 ppm. With Pomarsol in the range of 500 to 1500 ppm and for the both strains, the progeny was decreased by about 60%. A very reduced size and a leg paralysis was observed with each toxic powder for Oregon and triploid flies. It appears that a triploid stock of chromosomes does not significantly modify the reaction of the flies.

Transformation of erythroid cells by rous sarcoma virus (RSV)

RSV transforms several nonhematopoietic cell types and as reported here also has the capacity to transform hematopoietic cells of the erythroid lineage. In vitro, the three RSV isolates tested induced erythroblast-like colonies in infected bone marrow cells that were distinguishable by size and cell arrangement from those induced by avian erythroblastosis virus (AEV). Also in contrast to AEV-transformed erythroblast cultures, isolated cell colonies induced by RSV required complex growth conditions in liquid medium similar to the in vitro conditions necessary for erythroblasts transformed by the acute leukemia virus E26. Temperature-shift experiments using temperature-sensitive ( ts) NY68 RSV revealed that when grown at the nonpermissive temperature (42°), mutant-infected cells became benzidine positive and partially differentiated into erythrocytes. Wild-type ( wt) RSV-transformed cells did not undergo similar changes. However, both wt RSV-, and to a greater extent, ts RSV-transformed cultures at the permissive temperature (37°) did contain populations of spontaneously differentiating erythroid cells signifying that the transforming activity of the virus did not fully arrest erythroid maturation. In addition, the RSV-transformed cells did express tyrosine kinase activity. When injected intravenously into birds, RSV induced an erythroblastosis-like disease similar to AEV but also caused fibrosarcomas and leg paralysis. These results show that RSV can alter the pattern of erythroid differentiation in a manner similar to, but distinct from, AEV and indicate that the tyrosine-specific pp60 src kinase is involved in erythroid cell transformation. Since the arc and erb B proteins share a significant amino acid homology, these data suggest that both may also share a common functional homology.