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PubMed1985

Adrenocortical metabolism and plasma corticosterone in soman intoxicated rabbits.

The organophosphate neurotoxin soman produced impairments in adrenocortical RNA and protein metabolism. Fasciculate and reticular cell RNA and protein contents were suppressed with sublethal to acutely lethal dosages (20, 30 and 40 micrograms/kg, s.c.) during the acute excitatory phase of intoxication and at 6-8 h post injection. All three dosages produced ca 90% inactivation of plasma cholinesterase. A transient elevation of plasma corticosterone occurred with 20 micrograms/kg soman whereas there was a protracted increase with 30 micrograms/kg. Corticosterone was not significantly elevated with 40 micrograms/kg, but death occurred at 13 +/- 4 min. Thus, the magnitude and/or nature of soman-induced metabolic impairments does not appear to prevent adrenal activation.

Adrenal Cortex↗
PubMed1991

Carbofuran-induced alterations (in vivo) in high-energy phosphates, creatine kinase (CK) and CK isoenzymes.

Male Sprague-Dawley rats administered with an acute sublethal dose of carbofuran (1.5 mg/kg, s.c.) developed the signs of peak hypercholinergic activity during 30-60 min. At this time, in hemidiaphragm muscle, a significant decrease in ATP (28%) and phosphocreatine (PC) (29%) occurred without concurrent change in AMP and creatine (CR). A significant decrease in the levels of total adenine nucleotides (ATP + ADP + AMP) (20%) and total creatine compounds (PC + CR) (17%) was evident. The decline in the corresponding ratios of ATP/ADP (26%), ATP/AMP (39%), and PC/CR (20%) was therefore suggestive of greater utilization of ATP and PC in response to their increased demand for high-frequency muscle fasciculations. The energy charge = ATP + 1/2 ADP/(ATP + ADP + AMP), an index of high-energy phosphate adequacy in hemidiaphragm, remained unchanged. A significant (p less than 0.01) increase in serum magnesium with no concurrent change in calcium was also evident. The observed higher activity (152%) of total CK (EC 2.7.3.2) in the serum induced by carbofuran was possibly a reflection of more than a twofold increase in CK-BB isoenzyme (CK-1) and 141% increase in CK-MM isoenzyme (CK-3), which also strengthens our findings of enhanced synthesis of ATP and PC. Increased levels of CK-MM isoenzyme in the brain (253%) and hemidiaphragm (195%); and depletion of CK-BB isoenzyme in the hemidiaphragm (0%), heart (42%), and brain (77%), and of CK-MB isoenzyme (CK-2) in the brain (4%) and hemidiaphragm (14%), appeared to be the major contributory factors leading to enhanced serum CK activity.

Adenine Nucleotides↗
PubMed1989

Neurophysiological study in chronic GM2 gangliosidosis (hexosaminidase A and B deficiency), with motor neuron disease phenotype.

We report the electrophysiological investigation of two adult cases with GM 2 gangliosidosis with hexosaminidase A and B deficiency. Superficial peroneal biopsy was obtained from one patient. The electrophysiological alterations of the peripheral nervous system were fasciculations, signs of collateral reinnervation and loss of motor units, decrease in sensory potential amplitude and increase in distal motor latency. Increase in N9-N13 interpeak latency of the somatosensory evoked potentials and an increase I-V interpeak latency of the brain-stem auditory potentials were evident in both cases. Visual evoked potentials were normal. Nerve biopsy showed a severe loss of myelinated fibers, especially of those with the largest diameter, with no signs of segmental demyelination, or remyelination. A tentative interpretation of our findings is given.

Action Potentials↗
PubMed1981

The significance of cyclic EEG changes in Creutzfeldt-Jakob disease: prognostic value of their course in 9 patients.

The diagnostic value of the EEG in Creutzfeldt-Jakob disease is based not only on the presence of a typical pattern of periodic discharges but also on the appearance of cyclic changes in the EEG. The pattern of the cyclic EEG changes was analysed in 9 patients with Creutzfeldt-Jakob disease. The changes appear when the level of wakefulness is reduced. The alternating pattern rate increases as the disease progresses and accounts for as much as 100 per cent of the tracing when the patient is in coma. During the cyclic changes the cardiorespiratory rate is always higher in phase A than in phase B. Hypertonic fits and most myoclonic jerks are present only in the A-phase, whereas partial myoclonus and fasciculations are present in both phases. The cyclic change pattern in Creutzfeldt-Jakob disease reveals a progressive. The cyclic change pattern in Creutzfeldt-Jakob disease reveals a progressive, serious involvement of the waking system.

Aged↗
PubMed1988

Optic nerve hypoplasia associated with pupillary light-near dissociation, spastic paraparesis and other non-ocular anomalies.

We report a case of bilateral optic nerve hypoplasia in a patient with pupillary light-near dissociation, spastic paraparesis with deep hyperreflexia, mild distal hypotrophy especially of lower limbs, bilateral pes cavus and signs of motor peripheral neuropathy. Other associated signs were rhinolalia, hypotrophy and fasciculations of the tongue and cardiomyopathy. We differentiate the condition from a number of hereditary ataxias and paraplegias. The clinical features of Strümpell-Lorrain spastic paraplegia and amyotrophic lateral sclerosis seem to resemble most closely that of our patient.

Abnormalities, Multiple↗
PubMed1996

Neuron-specific expression of a chicken gicerin cDNA in transient transgenic zebrafish.

Gicerin, a novel cell adhesion molecule which belongs to the immunoglobulin superfamily, is expressed temporally and spatially in the developing chick brain and retina. The previous in vitro experiments using transfected cells showed that gicerin can function as a cell adhesion molecule which has both homophilic and heterophilic binding activities. For the in vivo analyses of gicerin in neural development, we tried to utilize a zebrafish system, a vertebrate suitable for studying early development. We generated transient transgenic animals by microinjecting DNA constructs into zebrafish embryos. Chicken gicerin, under control of the neurofilament gene promoter, was preferentially expressed in neuronal cells and gicerin-expressing neurons exhibited a fasciculation formation with neighboring gicerin-positive axons, which may be partly due to homophilic cell adhesion activity of gicerin. These experimental results suggest that this fast and efficient transgenic animal system is useful for studying the functional roles of neuron-specific genes during the development.

Animals↗
PubMed2004

Progressive bulbur paralysis (Fazio-Londe disease).

Progressive bulbar paralysis of childhood is characterised by progressive paralysis of muscles innervated by cranial nerves. The authors report a case of progressive bulbar paralysis of childhood in a 12-year-old child. Child was admitted with the complaints of drooping of eyelids, difficulty in swallowing and hoarse voice. She had involvement of III, VII, IX, X, XI and XII cranial nerves and the corticospinal tracts. Electromyography revealed spontaneous activity in the form of fasciculations, giant motor unit potential and discrete recruitment of motor neurons suggestive of denervation pattern. Hearing assessment was normal. Muscle biopsy was also suggestive of neurogenic atrophy.

Biopsy, Needle↗
PubMedDate not supplied

Molecular correlates of neuronal specificity in the developing insect nervous system.

The development of the nervous system in insects, as in most other higher animals, is characterized by the high degree of precision and specificity with which synaptic connectivity is established. Multiple molecular mechanisms are involved in this process. In insects a number of experimental methods and model systems can be used to analyze these mechanisms, and the modular organization of the insect nervous system facilitates this analysis considerably. Well characterized molecular elements involved in axogenesis are the cell-cell adhesion molecules that underlie selective fasciculation. These are cell-surface molecules that are expressed in a regional and dynamic manner on developing axon fascicles. Secreted molecules also appear to be involved in directing axonal navigation. Nonneuronal cells, such as glia, provide cellular and noncellular substrates that are important pathway cues for neuronal outgrowth. Once outgrowing processes reach their general target regions they make synapses with the appropriate postsynaptic cells. The molecular mechanisms that allow growth cones to recognize their correct target cells are essential for neuronal specificity and are being analyzed in neuromuscular and brain interneuron systems of insects. Candidate synaptic recognition molecules with remarkable and highly restricted expression patterns in the developing nervous system have recently been discovered.

Animals↗
PubMed1993

Are the glypiated adhesion molecules preferentially targeted to the axonal compartment?

The question of how the cell surface molecules may be specifically delivered to subdomains of neurons is of particular interest considering that polarized sorting to the axon could enable adhesion glycoproteins to induce fasciculation of axonal tracts, guidance to the target cell, and the establishment of synaptic contacts. It was recently proposed that GPI-anchored molecules undergo preferential delivery to the axonal surface, implicating a similar polarized sorting of glycoproteins in neurons and epithelial cells (Dotti and Simons, 1990; Dotti et al., 1991). This review focuses on the cellular and subcellular localization of several glypiated adhesion molecules (Thy-1, TAG-1, F3/F11, P-31) in the developing and adult cerebellar cortex of the mouse. We conclude that the cellular distribution of GPI-anchored adhesion molecules within neurons is very complex and depends on: 1. The neuronal cell types, for example, F3/F11 is localized in axons in granule cells but is present in all compartments of Golgi cells. 2. The molecule itself: Thy-1, TAG-1, and P-31 are present on the granule cell body, whereas at the same developmental stage, F3/F11 is restricted to the axon. 3. The differentiation state: Thy-1 delivery to the axon correlates with postsynaptic target maturation.

Animals↗
PubMed1977

An evaluation of the anaesthetic techniques used in an outpatient unit.

Our follow-up of 250 gynaecology patients and 100 dental patients who had received anaesthesia for elective outpatient surgical procedures indicates: (1) The practice of outpatient anaesthesia in proper facilities with proper selection of patients appears to be safe. (2) There is widespread patient acceptance of surgery and anaesthesia on an outpatient basis. (3) Complications are frequent but minor. (4) Many of the complications may be minimized: (i) Adequate depth of anaesthesia preferably with a volatile agent will do away with awareness during operation. (ii) Methoxyflurane should be avoided to minimize late arousal. Volatile agents such as enflurane or halothane would seem to be preferable to intravenous agents. (iii) Post-fasciculation pain could be minimized by avoiding succinylcholine for short procedures like D & C and using adequate depth instead. For dental procedures requiring tracheal intubation, one could perhaps use non-depolarizing muscle relaxants, like pancuronium, with reversal at the end of the procedure. (5) Nausea, vomiting, dizziness and headache are complications that occur very frequently in all series reported and this is an area where more research is indicated.

Abortion, Therapeutic↗
PubMed1976

Changes in plasma potassium and calcium levels and in the electrocardiogram after a single dose of succinylcholine preceded by d-tubocurarine.

One hundred and eighteen patients undergoing surgical procedures not requiring immediate tracheal intubation, nor producing visceral reflexes, were pretreated with d-tubocurarine 6 mg, three minutes before the administration of a bolus of succinylcholine (2 mg/kg). Electrocardiographic changes, venous and arterial plasma potassium and calcium levels, CPK changes (12 patients) and appearance of myoglobinuria (35 patients) were followed. Pretreatment with a small dose of d-tubocurarine did not change the overall incidence and pattern of arrhythmias; it did, however, prevent increases in plasma potassium in 90.4 per cent of the patients, mean plasma potassium values remaining below pre-induction levels. The CPK level changed in only one of 12 patients (from 10 to 21 I.U., the normal range being 0 to 34 I.U.). No myoglobinuria was detected in any of the patients tested. A rapid but short-lasting change in the K+/Ca++ ratio did not seem to influence the occurrence of arrhythmias. Pretreatment with a small dose of d-tubocurarine is effective in preventing or decreasing fasciculations, plasma potassium and CPK changes and myoglobinuria described after the intravenous administration of succinylcholine. The already useful role of succinylcholine in our armamentarium can be made safer by pretreatment with a small dose of d-tubocurarine.

Adolescent↗
PubMed1977

Characteristics of nondepolarizing neuromuscular block: (I) post-junctional block by alpha-bungarotoxin.

The characteristics of neuromuscular block produced by alpha-bungarotoxin, a post-junctionally active polypeptide toxin purified from snake venoms, have been studied in vivo in 12 anaesthetized cats, using the sciatic nerve-tibialis anterior muscle preparation. The onset of the neuromuscular block was slow and without fasciculation. The block was persitently progressive. The time course of the block depended on the dosage. In general, 0.1 mg/kg of alpha-BuTX appeared to approximate the threshold dosage while 0.2 mg/kg completely eliminated the twitch response in 2-5 hours. No recovery was observed in 8-30 hours. Larger doses accelerated the progression of the block. During the block, tetanic contractions and train-of-four twitches did not fade. The post-tetanic twitches were markedly facilitated. The block was antagonized by edrophonium, neostigmine, pyridostigmine, and succinylcholine, but the antagonism was less effective and shorter-lasting than that observed on curare-block, and the block always resumed the projected progression. Attempts were made to explain the observed difference between alpha-BuTX- and dTc-induced neuromuscular blocks by the practically permanent nature of block and the purely post-junctional site of action of alpha-BuTX. It was concluded that a pure post-junctional block is not characterized by fade, which rather might be a pre-junctional effect of some nondepolarizing neuromuscular blocking agents like d-tubocurarine.

Animals↗
PubMed1982

Cardiac effects of self-taming of succinylcholine and repeated succinylcholine administration.

Pretreatment with small (10 mg) doses of succinylcholine ("self-taming") decreases the incidence of muscle fasciculations following succinylcholine administration and may decrease the incidence of other unwanted effects. This study was designed to assess the cardiac effects of such self-taming and to assess the degree of protection afforded against bradydysrhythmias following subsequent succinylcholine administration. Sixty patients were studied and allocated randomly to three groups of twenty. Each group was assigned a different form of pretreatment. Patients in group I received 10 mg of succinylcholine immediately after induction. Patients in group II were treated with d-tubocurarine 0.04k mg . kg-1 three minutes before induction. Patients in group III received no pretreatment. All patients were induced with thiopentone 4 mg . kg-1 followed by succinylcholine 1 mg . kg-1 45 seconds later. A second dose of succinylcholine 1 mg . kg-1 was administered to the patients in the two pretreatment groups between four and five minutes after the first dose of succinylcholine. Following both the first and second doses of succinylcholine patients in the self-taming group showed a significantly greater incidence of bradydysrhythmias when compared to the other two groups. It is concluded that the use of a self-taming technique is potentially hazardous, and that it does not confer protection against repeated succinylcholine administration.

Anesthesia↗
PubMed1996

Sevoflurane anaesthesia for a patient with adult polyglucosan body disease.

PURPOSE: Adult polyglucosan body disease (APBD) is a rare neurological disorder of unknown cause characterized by four manifestations: upper motor neuron signs, peripheral neuropathy with motor and sensory loss, urinary incontinence, and dementia. The purpose of this report is to present a patient with APBD anaesthetized successfully with sevoflurane and nitrous oxide. CLINICAL FEATURE: A 51-yr-old man with APBD was scheduled for haemorrhoidectomy. Paraesthesia, dysaesthesia, distal muscular atrophy and fasciculation were recognized in the extremities. Dementia, bulbar paralysis and respiratory insufficiency were basent. Anaesthesia was induced with inhalation of sevoflurane and nitrous oxide, and the trachea was intubated without the use of muscle relaxants. Maintenance of anaesthesia was performed with sevoflurane (inspired concentration: 1.5-2.5%) and nitrous oxide (50%). Emergence from anaesthesia and the postoperative course were uneventful, and no exacerbation of neurological signs and symptoms was recognized. No postoperative analgesia was required. CONCLUSION: General anaesthesia and tracheal intubation with sevoflurane and nitrous oxide provided safe anaesthesia for a patient with APBD.

Anesthesia↗
PubMed1984

Succinylcholine-induced cardiac arrest in unsuspected Duchenne muscular dystrophy.

A case history is presented of a three-year-old boy with unsuspected Duchenne muscular dystrophy, who suffered a cardiac arrest following the administration of a single dose of succinylcholine during a halothane anaesthetic. The arrest was associated with lack of fasciculations, muscle rigidity, hyperkalemia, myoglobinuria, and massive elevation of serum creatine phosphokinase. Asystole was prolonged and refractory to treatment, although cardiac activity was eventually restored. The possible cause of the circulatory collapse is discussed and reports of similar cases reviewed. Neither succinylcholine nor halothane should be employed in cases with known or suspected Duchenne muscular dystrophy.

Child, Preschool↗
PubMed1999

[Hypokalemic paralysis in furosemide therapy and simultaneous laxative abuse].

BACKGROUND: Clinical signs of hypokalemia are not directly related to the extent of the electrolyte imbalance, and therefore monosymptomatic cases may be observed. CASE REPORT: Following an acute gastroenteritis with considerable diarrhea, a 47-year-old male patient was admitted to hospital for progressive painful paraparesis. Upon admission, the patient complained of painful paresthesias in both legs, and a moderate flaccid paraparesis with widespread fasciculations and loss of leg tendon reflexes was found. Serum potassium level on admission was 1.7 mmol/l. Other signs of hypokalemia were absent, and the ECGs showed a slow sinus rhythm without disturbances of de- or repolarisation or cardiac arrhythmias. Hypokalemic paralysis was diagnosed and was considered to be primarily drug-induced, as the patient had a history of laxative abuse and was on a continuous medication with furosemide (80 mg/d) without regular assessment of serum electrolytes. The additional electrolyte loss following the gastroenteritis precipitated the development of clinical signs of hypokalemia. In parallel to the rise in serum potassium levels, both painful paresthesias and muscle weakness disappeared, and electromyography documented the amelioration of the myopathic syndrome. CONCLUSION: The prominent clinical symptom of hypokalemia was a dyskalemic paralysis in the absence of other sequelae of electrolyte imbalance, such as cardiac arrhythmias or vegetative disturbances.

Cathartics↗
PubMed1999

ISIS Survey: an international study on the diagnostic process and its implications in amyotrophic lateral sclerosis.

In a number of ALS patients, a long delay between onset of symptoms and diagnosis is reported. In this international study (ISIS Survey) we have identified the pathway followed by ALS patients from first symptoms to diagnosis confirmation. Diagnostic data from a total of 201 patients with definite ALS from 6 countries (Argentina, Brazil, Germany, Italy, Spain and the USA) were analyzed. The median time needed to confirm diagnosis was found to be 14 months; time to first consultation took 2 months, time to consultation with a neurologist took 8 months, and time for observation and diagnostic assessment by the neurologist took 4 months. This time delay was shorter when presentation was at bulbar level and when fasciculations were present. The major causes of diagnostic delay were unfamiliarity of the physician with the disease, unusual clinical presentation, coexistence of other diseases to which clinical symptomatology was attributed, misleading findings or misinterpretation of neuro-radiological or neurophysiological findings. The diagnostic delay has several implications for patients and their families, including mismanagement, delay in establishing appropriate and individualized pharmacological and symptomatic therapies, and difficulty in planning personal and familiar future.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

Adverse reactions and interactions of the neuromuscular blocking drugs.

The adverse reactions seen following administration of neuromuscular blocking agents are mainly cardiovascular. Due to the lack of specificity for the nicotinic receptor at the neuromuscular junction, these agents may interact with receptors in autonomic ganglia and muscarinic receptors in the heart. Furthermore, muscle relaxants may have histamine-releasing properties. The cardiovascular effects vary with potency and specificity of the drug, depending mainly on the chemical structure. Pancuronium, fazadinium and especially gallamonium block cardiac muscarinic receptors, and tachycardia may be seen. Atracurium, metocurine and in particular d-tubocurarine have histamine-releasing properties and may cause flushing, hypotension and tachycardia. Vecuronium has no effect on the cardiovascular system. The effect of succinylcholine on heart rate differs between children, where bradycardia is seen, and adults in whom tachycardia may follow. However, bradycardia may occur in adults following a single dose. Succinylcholine increases plasma potassium, especially in patients with nerve damage, and arrhythmias may be observed. The neuromuscular adverse effects of succinylcholine, such as fasciculations and increased gastric and intraocular pressure, may be prevented by precurarisation. Many drugs interact with neuromuscular blocking agents and there is often a potentiation of the neuromuscular effect. This is of clinical importance in the case of antibiotics, inhalational anaesthetics, lithium and cyclosporin. Difficulty in reversing the block may occur with calcium channel blockers and polymyxin. However, some drugs, such as phenytoin, carbamazepine and lithium, may cause resistance to neuromuscular blocking agents. Furthermore, clinically important interactions exist between individual neuromuscular blocking drugs. Precurarisation with a non-depolarising drug prolongs the onset of succinylcholine, and conversely a prolonged effect of non-depolarising drugs is seen following succinylcholine. The effect of succinylcholine is markedly prolonged if the drug is administered during recovery from pancuronium blockade or following neostigmine for reversal. Succinylcholine is hydrolysed by plasma cholinesterase, and drugs which decrease the activity of this enzyme may produce a prolonged block, i.e. contraceptive pills, cyclophosphamide, echothiopate and organophosphate.

Drug Interactions↗