Medulloblastoma induces unusual headache with clinical picture of basilar-type migraine complicated by ischaemic infarcts.
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Publications and source records attributed to A Cannas.
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We report the case of a patient who developed notalgia paresthetica during the recovery from a neuralgic amyotrophy. A 23-year-old woman had a typical neuralgic amyotrophy (severe shoulder pain, followed by a long thoracic nerve palsy); five months after the onset of pain, when scapular winging was improving, she began to feel a burning sensation in a restricted interscapular area, on the same side. Electromyography was consistent with a long thoracic nerve neuropathy, with minor neurogenic changes in deltoid and biceps brachii. Radiography of the spine was unremarkable. The notalgia paresthetica disappeared shortly before the complete recovery of scapular winging. The abnormal activation of shoulder girdle and spine extensor muscles during the time of long thoracic nerve palsy may explain the association between the two disorders.
A woman with a history of spine injury in her remote past developed Brown-Sequard syndrome due to a thoracic transdural spinal cord herniation. A clue about the underlying mechanism was offered by the unexpected imaging feature of a nuclear trail sign just below the herniated cord. As suggested by Watters et al., who reported a similar case, this finding is consistent with the hypothesis that intrathecal rupture of disk material could have resulted in an acquired tear of the ventral dural, through which the cord herniated.
The Cornell Net Carbohydrate and Protein System (CNCPS), a mechanistic model that predicts nutrient requirements and biological values of feeds for cattle, was modified for use with sheep. Published equations were added for predicting the energy and protein requirements of sheep, with a special emphasis on dairy sheep, whose specific needs are not considered by most sheep-feeding systems. The CNCPS for cattle equations that are used to predict the supply of nutrients from each feed were modified to include new solid and liquid ruminal passage rates for sheep, and revised equations were inserted to predict metabolic fecal N. Equations were added to predict fluxes in body energy and protein reserves from BW and condition score. When evaluated with data from seven published studies (19 treatments), for which the CNCPS for sheep predicted positive ruminal N balance, the CNCPS for sheep predicted OM digestibility, which is used to predict feed ME values, with no mean bias (1.1 g/100 g of OM; P > 0.10) and a low root mean squared prediction error (RMSPE; 3.6 g/100 g of OM). Crude protein digestibility, which is used to predict N excretion, was evaluated with eight published studies (23 treatments). The model predicted CP digestibility with no mean bias (-1.9 g/100 g of CP; P > 0.10) but with a large RMSPE (7.2 g/100 g of CP). Evaluation with a data set of published studies in which the CNCPS for sheep predicted negative ruminal N balance indicated that the model tended to underpredict OM digestibility (mean bias of -3.3 g/100 g of OM, P > 0.10; RMSPE = 6.5 g/100 g of OM; n = 12) and to overpredict CP digestibility (mean bias of 2.7 g/100 g of CP, P > 0.10; RMSPE = 12.8 g/100 g of CP; n = 7). The ability of the CNCPS for sheep to predict gains and losses in shrunk BW was evaluated using data from six studies with adult sheep (13 treatments with lactating ewes and 16 with dry ewes). It accurately predicted variations in shrunk BW when diets had positive N balance (mean bias of 5.8 g/d; P > 0.10; RMSPE of 30.0 g/d; n = 15), whereas it markedly overpredicted the variations in shrunk BW when ruminal balance was negative (mean bias of 53.4 g/d, P < 0.05; RMSPE = 84.1 g/d; n = 14). These evaluations indicated that the Cornell Net Carbohydrate and Protein System for Sheep can be used to predict energy and protein requirements, feed biological values, and BW gains and losses in adult sheep.
NcSAG1 and NcSRS2, the two major immunodominant tachyzoite surface antigens of the apicomplexan parasite Neospora caninum, were investigated for their potential as vaccine candidates in mice. Recombinant recNcSRS2 and recNcSAG1 were expressed in Escherichia coli as poly-histidine-tagged fusion proteins. Separate groups of mice were immunized with purified recNcSAG1, recNcSRS2, or a combination of both, and were then challenged with N. caninum tachyzoites. Subsequent experiments included intramuscular vaccination of mice with the eukaryotic expression plasmid pcDNA3 containing either NcSRS2 or NcSAG1 cDNA inserts, followed by a single booster with the corresponding recombinant antigens. Immunization with a crude somatic antigen (NC1-extract) was included in the experiments. Following challenge, the presence of the parasite in the different organs was assessed by a N. caninum-specific PCR, while the parasite burden in infected brain tissue was assessed by quantitative real-time PCR. Immunization of mice employing individual recombinant antigens, or combined recNcSAG1/recNcSRS2, resulted in a lower degree of protection against cerebral infection, when compared to combined DNA/recombinant antigen vaccination. Serological analysis showed that this protective effect was associated with the occurrence of antibodies directed against native parasite antigens in those animals receiving combined DNA/recombinant antigen vaccination. Conversely, mice immunized with recombinant antigens alone generated antibodies recognizing only the recombinant antigens. Mice experiencing clinical signs such as walking disorders, rounded back, apathy and paralysis were observed only in the untreated positive control groups, but never in the vaccinated groups. Our results suggest that a combined DNA/recombinant antigen-vaccine, based on NcSAG1 and NcSRS2, respectively, exhibited a highly significant protective effect against experimentally induced cerebral neosporosis in mice.
Two experiments were conducted to study the amount of aflatoxin M1 (AFM1) in milk in response to feeding aflatoxin B1 (AFB1). In experiment 1, four dairy ewes in early lactation received a single dose of pure AFB1 (2 mg). Individual milk samples were collected during the following 5 d to measure AFM1 concentration. The average excretion of AFM1 in milk followed an exponential decreasing pattern, with two intermediate peaks at 24 and 48 h. No AFM1 was detected in milk at 96 h after dosing. The mean rate of transfer of AFB1 into AFM1 in milk was 0.032%, with a high individual variability (SD = 0.017%). In experiment 2, 16 dairy ewes in midlactation were divided into four groups that received different daily doses of AFB1 (0, 32, 64, and 128 microgram for control and groups T1, T2, and T3, respectively) for 14 d. Pure AFB1 was administered to each animal divided in two daily doses. Individual milk samples were collected at 12, 24, 36, 48, 72, 96, 144, 216, and 312 h after the first AFB1 administration, during the intoxication period, and every 24 h for 7 d after the withdrawal of AFB1. AFM1 was detected in the milk of all animals of the treated groups at 12 h after the administration of AFB1. In all treated groups, milk AFM1 concentration increased from 12 to 144 h after the beginning of administration. It then decreased, reaching a stable concentration at 216 and 312 h after the first administration. No AFM1 was detected in milk 3 d after the last administration of AFB1. Milk AFM1 concentration measured at steady-state condition was significantly affected by the AFB1 dose (0.031, 0.095, and 0.166 in T1, T2, and T3 groups, respectively), with a linear relationship between AFB1 dose and milk AFM1 concentration (R2 = 77.2%). The carryover (AFM1/AFB1 ratio) was not significantly affected by treatment, and its mean value was 0.112% (SE = 0.011). The carryover was lower than that reported for dairy cattle and goats, suggesting a better ability of sheep to degrade AFB1.
Five patients (4 women) with Parkinson's disease (PD) and primary major psychiatric disorder (PMPD) meeting DSM-IV criteria for the diagnosis of bipolar affective disorder (BAD) were studied. Four patients had early onset PD. Four developed a severe psychiatric disorder a few years after starting dopaminergic therapy in presence of a mild motor disability and a mild cognitive impairment, with no evidence of cerebral atrophy at CT or MRI. Two patients developed a clear manic episode; the other three presented a severe depressive episode (in one case featuring a Cotard syndrome). None showed previous signs of long term L-dopa treatment syndrome (LTS), hallucinosis or other minor psychiatric disorders. The two manic episodes occurred shortly after an increase of dopaminergic therapy and in one case rapid cyclic mood fluctuations were observed. At the onset of psychiatric symptoms, all patients had an unspecific diagnosis of chronic delusional hallucinatory psychosis (CDHP).
Neosporosis is a disease affecting predominantly fetal development in cattle and dog hosts; and it may cause neuromuscular disfunction in infected newborn calves and pups. Predispositions--including, e.g. transient immunosuppression during pregnancy--may result in an increased dissemination of the parasite within the host or its offspring. Chemotherapeutic treatment of neosporosis may be an issue, provided that an appropriate drug is made available. In this respect, we describe the use of a mouse model for the evaluation of toltrazuril and ponazuril medication as a means of preventing parasite dissemination and subsequent formation of cerebral lesions. Toltrazuril- and ponazuril-treated mice were experimentally infected intraperitoneally (i.p.) with 2 x 10(6) Neospora caninum tachyzoites. The infection was monitored at three levels: clinically, by assessing symptoms, histologically, by assessing the occurrence of cerebral lesions and parasites by immunohistochemistry, and on the molecular level, by detection of parasite DNA using PCR. Chemotherapy using either toltrazuril or ponazuril, both applied in a drinking-water formulation (20 mg toltrazuril or ponazuril kg(-1) body weight day(-1)) completely prevented the formation of cerebral lesions in all treated animals, as assessed by immunohistochemistry. PCR analyses of these treated animals showed that DNA-detectability was reduced by 91% and 90% upon toltrazuril and ponazuril medication, respectively.
Chronic delusional psychosis with hallucinations (CDHP) is commonly assumed to complicate the later stages of Parkinson's disease, as a side effect of antiparkinsonian medication. We studied 7 patients with early onset PD, who had developed psychiatric manifestations consisting in CDHP after a few years of antiparkinsonian therapy. All patients underwent a neurological, psychiatric and brain imaging (CT or MRI) evaluation. Detailed clinical history was recorded in order to reveal prior psychiatric illness and to analyse the relationship between neurological disease, cognitive impairment and psychosis. Our findings suggest that CDHP occurring in patients with early onset PD, normal or slightly impaired cognitive functions and normal CT/MRI scans is invariably the expression of a coexisting psychiatric illness which prior to onset of the neurologic disease had not been correctly diagnosed and which has been disclosed by dopaminergic therapy.
In apicomplexan parasites, host cell adhesion and subsequent invasion involve the sequential release of molecules originating from secretory organelles named micronemes, rhoptries, and dense granules. Microneme proteins have been shown to be released at the onset of the initial contact between the parasite and the host cell and thus mediate and establish the physical interaction between the parasite and the host cell surface. This interaction most likely involves adhesive domains found within the polypeptide sequences of most microneme proteins identified to date. NcMIC3 is a microneme-associated protein found in Neospora caninum tachyzoites and bradyzoites, and a large portion of this protein is comprised of a stretch of four consecutive epidermal growth factor (EGF)-like domains. We determined the subcellular localization of NcMIC3 prior to and following host cell invasion and found that NcMIC3 was secreted onto the tachyzoite surface immediately following host cell lysis in a temperature-dependent manner. Surface-exposed NcMIC3 could be detected up to 2 to 3 h following host cell invasion, and at later time points the distribution of the protein was again restricted to the micronemes. In vitro secretion assays using purified tachyzoites showed that following secretion onto the surface, NcMIC3 was largely translocated towards the posterior end of the parasite, employing a mechanism which requires a functional actin microfilament system. Following this, the protein remained bound to the parasite surface, since it could not be detected in a soluble form in respective culture supernatants. Secretion of NcMIC3 onto the surface resulted in an outward exposure of the EGF-like domains and coincided with an increased capacity of N. caninum tachyzoites to adhere to Vero cell monolayers in vitro, a capacity which could be inhibited by addition of antibodies directed against the EGF-like domains. NcMIC3 is a prominent component of Triton X-100 lysates of tachyzoites, and cosedimentation assays employing prefixed Vero cells showed that the protein binds to the Vero cell surface. In addition, the EGF-like domains, expressed as recombinant proteins in Escherichia coli, also interacted with the Vero cell surface, while binding of NcSRS2 and NcSAG1, the major immunodominant surface antigens, was not as efficient. Our data are indicative of a functional role of NcMIC3 in host cell infection.
Painful tonic spasms (PTS) are now regarded as a typical symptom of multiple sclerosis but pathologic or radiologic findings rarely have been described. We report clinical and magnetic resonance imaging records of five original cases. In all of them, lesions likely responsible for unilateral PTS involved the motor pathway at the level of the posterior limb of the internal capsule or the cerebral peduncle on the opposite side. Closeness of motor fibers seems to be the most important underlying anatomic factor because it enables involvement of a higher proportion of axons by a single demyelinating lesion and radial spread of ephaptic activation. In turn, preservation of the underlying pyramidal-spinal tract could make it easier for the pathologic discharge to reach the peripheral effectors and generate PTS.
OBJECTIVE: A new surgical approach to foraminal disc herniation is proposed. METHODS: The procedure was performed in 28 patients during a span of 3 years. The herniation was purely foraminal in 18 patients and mainly foraminal with a definite extraforaminal component in the other 10 patients. Surgical treatment was offered only after 6 weeks of therapy with anti-inflammatory drugs and strict bed rest had proved to be ineffective. SURGICAL TECHNIQUE: To unroof the foraminal compartment, an ovoid fenestration (10 x 5 mm) is cut, with its major longitudinal axis at the level of the pars interarticularis, just medially and slightly off-center under the lateral isthmic notch, i.e., below the pedicle projection. This fenestration exposes the foraminal root compressed by the herniated disc, which can be easily removed. RESULTS: Treatment was successful in all patients, with swift remission of pain and only mild postoperative discomfort. All patients resumed their occupations as usual within 10 to 30 days after the operation, according to type of work. Mean follow-up is 24 months (range, 12-36 mo), without any return of pain. CONCLUSION: We propose pars interarticularis fenestration because it spares, with minimal bone removal, the facet joints and the anatomic continuity of the pars interarticularis, yet properly exposes the foraminal compartment both medially and laterally and thereby permits optimal removal of the disc herniation.
Sclerosteosis is a rare genetic disorder of bone modelling, similar to, but distinct from, van Buchem disease; it has been described almost exclusively in Afrikaners of South Africa, a white population of Dutch ancestry. Isolated cases have been reported in a girl in Japan, a boy in Spain, and in multiracial families in Brazil and USA. Here we report a case of sclerosteosis in a black man born in Senegal. He presented with the full features of the disease: tall stature; syndactyly: nail dysplasia; massive sclerosis of the long tubular bones, the ribs, the pelvis and the skull; multiple cranial nerve involvement: optic atrophy, facial palsy and trigeminal neuralgia. Radiologic examination, visual and brainstem auditory evoked potentials, computerized tomography and magnetic resonance imaging of the skull were performed. This seems to be the first case of the disease in a black African individual, with no known relationship with Dutch ancestry.
To study the effects of dietary crude protein (CP) and energy on milk urea N concentrations in dairy sheep, eight pelleted total mixed rations were prepared to obtain two levels of energy density (1.65 and 1.55 Mcal of net energy for lactation per kilogram of dry matter for high energy and low energy rations, respectively) and four concentrations of CP within each energy level (mean CP concentrations, 14.0, 16.4, 18.7, and 21.2% of dry matter). The experimental design consisted of two 4 x 4 Latin squares (one per energy level) with two replications per treatment within each 3-wk period. Milk urea N concentrations were similar between dietary energy levels. Within each energy level, milk urea N was linearly and positively associated with dietary CP content and intake (range of milk urea N concentrations, 12.2 to 25.8 mg/dl for ewes fed high energy rations and 12.9 to 26.7 mg/dl for ewes fed low energy rations). The comparison of these results with those from other trials suggested that milk and blood urea N concentrations are closely correlated with dietary CP concentrations and less closely correlated with dietary CP intake. Our results suggest that milk or blood urea N concentrations can be used as indicators of protein metabolism and intake of lactating ewes.
Visual Evoked Potentials (VEP) were measured in 9 new-diagnosed hypothyroid female patients--mean age 46 +/- 12 ys--before treatment, during (with monthly evaluations) thyroid hormone replacement therapy and after long-term therapy, at the achievement as well as one year after having achieved and maintained euthyroidism. Three of the hypothyroids had abnormally prolonged latencies (m.v. 131.7 +/- 7.9 ms), while 7 had lower than normal amplitude (m.v. 2.3 +/- 2.8 microV). No remarkable change of amplitude was observed after the achievement of euthyroidism, after a mean time of 5.9 +/- 4.9 months (range 2-14 months). A significant shortening of latency (m 128.3 +/- 7.6 ms), even still higher than the control value (m 122.7 +/- 3.7 ms) was found. Significant correlation between P100 latency and thyroid hormone levels was found for TT4 (r = 0.3353; p = 0.005), TT3 (r = 0.2568; p = 0.032) and FT4 (r = 0.3572; p = 0.002). No further improvement in P100 latency (m 129.5 +/- 7.2 ms; p = 0.037) was found one year after the achievement of euthyroidism, while a remarkable amplitude increase (m 9.2 +/- 3.4 micro; p = 0.001) was observed. Our findings indicate that, as well as other studied parameters, VEP are reversibly alterated in hypothyroidism, probably in relation to metabolic rather than to structural alterations. Moreover, VEP can represent a useful neurophysiologic parameter for quantitation of SNC involvement in hypothyroidism.
Interferon (IFN)-gamma increases the sensitivity of tumor cell lines, many of which are p53 mutants, to tumor necrosis factor-alpha-mediated and anti-Fas antibody-mediated cell death. To better understand the mechanism of IFN-gamma action in modulating the cell death response independently of p53 function, we analyzed the death of the human colon adenocarcinoma cell line, HT-29, following treatment with IFN-gamma and various cytotoxic agents. Here we show that IFN-gamma modulates cell death by sensitizing the cells to killing by numerous pro-apoptotic stimuli but not pro-necrotic stimuli. Furthermore, we show that select genes from several important apoptosis-related gene families are induced by IFN-gamma, including the apoptosis-signaling receptors CD95 (Fas/APO-1) and TNFR 1 and interleukin-1beta-converting enzyme (Ice) family members Ice, CPP32 (Yama, apopain), ICErel-II (TX, Ich-2), Mch-3 (ICE-LAP3, CMH-1), Mch-4, and Mch-5 (MACH, FLICE). Of the bcl-2 family members, IFN-gamma directly induced bak but notably not bax, which is activated by p53. The IFN-responsive transcriptional activator interferon regulatory factor-1 was also strongly induced and translocated into the nucleus following IFN-gamma treatment. We propose that IFN-gamma modulates a p53-independent apoptotic pathway by both directly and indirectly inducing select apoptosis-related genes.
We have recently demonstrated that a single injection of the mitogen lead nitrate to rats induced a rapid increase of tumor necrosis factor-alpha (TNF-alpha) mRNA in the liver and suggested that this cytokine may be involved in triggering hepatocyte proliferation in this model of direct hyperplasia. In this study, we examined whether a similar induction of liver TNF-alpha mRNA could be observed preceding the onset of hepatocyte proliferation induced by ethylene dibromide, another hepatocyte mitogen. In addition, we used dexamethasone, a well known inhibitor of TNF-alpha production, to determine whether its administration could suppress hepatocyte proliferation induced by lead nitrate and ethylene dibromide. A single intragastric administration of ethylene dibromide (100 mg/kg) to male Wistar rats enhanced liver TNF-alpha mRNA after 4 and 7 hours, which then returned to control levels by 24 hours. TNF-alpha mRNA was detectable only in a nonparenchymal cell fraction of the liver. Pretreatment of rats with a single dose of dexamethasone (2 mg/kg) 60 minutes before lead nitrate (100 mumol/kg) or ethylene dibromide completely abolished the increased levels of liver TNF-alpha mRNA induced by these agents. Inhibition by dexamethasone of TNF-alpha mRNA was associated with an inhibition of liver cell proliferation induced by these mitogens, as measured by [3H]thymidine incorporation into hepatic DNA, mitotic index, and DNA content. These results further support the hypothesis that TNF-alpha may be involved in triggering hepatocyte proliferation induced by primary mitogens.
The authors carried out an epidemiologic study on amyotrophic lateral sclerosis in Sardinia for the years 1957 through 1990. The duration of the disease and survival were significantly shorter in bulbar form. The distribution of ALS in various areas of the island was found to be not at all homogeneous. Mean yearly incidence showed no significant variations in the decades 1971-80 and 1981-90. In the last decade, an increase of bulbar forms was observed.