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Abstracts

Abstracts

Angina (Spasm)

Angina

Coronary spasm can be induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact by releasing nitric oxide (NO).

Coronary spasm is promptly relieved by nitroglycerin, which vasodilates through its conversion to NO. It is thus possible that NO release may be deficient in the spasm arteries in patients with coronary spastic angina (CSA).

Determined whether NO release is deficient in coronary arteries of patients with CSA.

There is a deficiency in endothelial NO activity in spasm arteries, which leads to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with CSA. This deficient endothelial NO activity plays an important role in the pathogenesis of coronary spasm.

Kugiyama K et al., Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina. Circulation, 94(3):266-71 1996 Aug 1.

Botulinum (Spasm)

Botulinum

Hemifacial spasm is nearly always a unilateral disease of the facial musculature and is characterized by involuntary tonic or clonic cramps that considerably reduce the affected patient's quality of life.

A number of different conservative and operative therapeutic procedures have been applied but often failed to control the disease, permanently, or resulted in unwanted, sometimes strong, side effects.

Botulinum therapy in 29 patients with hemifacial spasm (78 therapeutic sessions).

The mean duration of an effect after treatment with botulinum toxin was 18 weeks. Side effects were rare.

Subcutaneous application of toxin (Clostridium botulinum) to involved facial muscles represents a successful treatment of hemifacial spasm.

Laskawi R et al., Botulinum toxin treatment in patients with hemifacial spasm. Eur Arch Otorhinolaryngol, 1994, 251:5, 271-4.

Broncho-spasm Latex Allergy

Broncho-spasm Latex Allergy

These are three case studies of spina bifida children during surgery who had "allergic" reactions to latex. The first case was a 13 year old spina bifida patient undergoing her tenth surgical procedure who developed severe anaphylaxis and bronchospasms. She was discovered to have a latex "allergy" demonstrated by "skin" prick test and the test was much more positive for gloves sterilized with ethylene oxide. RAST ethylene oxide testing was very positive.

The next case was a 14 year old male undergoing his 24th surgery who developed anaphylaxis 40 minutes after surgery began. A skin test utilizing an epidermal "puncture" from a drop of latex emulsion was very strongly positive. Sterilized gloves with gamma rays or ethylene oxide gave a more definite reaction. RAST testing was positive for latex but negative for ethylene oxide.

The last case was a nine year old female who had undergone 10 previous surgeries without problems who required catheterization four times daily using latex catheters sterilized with ethylene oxide. She developed "tachycardia", decreased "blood pressure" and a generalized "erythematous" "rash" during a surgical procedure. Prick tests for latex were positive. RAST tests for latex and ethylene oxide were positive.

Recommend the avoidance of latex urinary catheters and other equipment sterilized with ethylene oxide for children with spina bifida during surgical procedures or daily catheterization. Alternatives are available. Prick and RAST tests are reliable for detecting latex allergy and they are easy to perform. The authors suggest these be routinely done in children with spina bifida before a new surgical procedure is implemented.

"Allergic Shock To Latex and Ethylene Oxide During Surgery For Spina Bifida", Moneret-Vautrin, D.A., et al, Anesthesiology, September 1990;73(3):556-557.

Coronary Artery Spasm

Coronary Artery Spasm

The intracellular mechanism for coronary artery spasm is still unknown. Since the protein kinase C (PKC)-mediated pathway and Ca2+ release from sarcoplasmic reticulum (SR) are important intracellular mechanisms of vascular smooth muscle contraction, examined the possible role of these mechanisms in the pathogenesis of coronary spasm in our swine model in vivo.

Results suggest that:
1. PKC activation largely accounts for the serotonin- and histamine-induced coronary spasm;
2. at the spastic site, the calcium influx through L-type Ca2+ channels may be augmented via the PKC-mediated pathway; and
3. the Ca2+ release from the SR into the cytosol may not play a primary role in coronary spasm.

Kadokami T et al., Coronary artery spasm does not depend on the intracellular calcium store but is substantially mediated by the protein kinase C-mediated pathway in a swine model with interleukin-1 beta in vivo. Circulation, 94(2):190-6 1996 Jul 15.

Infantile (1)

Infantile (1)

Analyzed the magnitude of the risk factors for infantile spasms.

There was a family history of seizures in 14% of children with infantile spasms, 29% of children with other forms of epilepsy, 26% of children with febrile seizures, and 5% of children with CNS infections.

However, a family history of seizures increased the risk for infantile spasms only in the cryptogenic group.

Children with infantile spasms were significantly more likely to have cerebral palsy, microcephaly, hydrocephaly, CNS malformations, neonatal hypoxia, or neonatal seizures than children with other types of epilepsy, febrile seizures, or CNS infections.

There was a modest genetic predisposition to seizures in children with infantile spasms. However, a much stronger association with underlying neurologic abnormalities, mainly neonatal seizures, neonatal hypoxia, and CNS malformations.

Rantala H et al., Risk factors of infantile spasms compared with other seizures in children under 2 years of age. Epilepsia, 37(4):362-6 1996 Apr.

Infantile (2)

Infantile (2)

A new combination therapy, high-dose pyridoxal phosphate (40 to 50 mg/kg daily) and low-dose corticotropin (0.01 mg [0.4 IU]/kg daily), was tried in 28 children with infantile spasms.

Monotherapy with pyridoxal phosphate provided excellent seizure control in three (11%) of the 28 subjects. Corticotropin was subsequently added to the regimen of the remaining 25 patients. At 1 month after discontinuing corticotropin, 21 (84%) of the 25 patients experienced no seizures, and 22 (88%) of the 25 showed improvement in their electroencephalographic findings.

The mean interval until achievement of seizure control was 4.1 days after the initiation of corticotropin. The outcome in the 21 patients has been followed for a mean period of 34.9 months (range, 2 to 81 months). Of these 21 patients, six (29%) have had relapses of infantile spasms, and 10 (48%) have experienced normal development.

Transient increases in liver enzymes occurred in 14 (50%) of the 28 patients, but none of the patients developed more serious side effects.

Takuma Y & Seki T: Combination therapy of infantile spasms with high-dose pyridoxal phosphate and low-dose corticotropin. J Child Neurol, 11(1):35-40 1996 Jan.

Infantile (3) - Tetany

Infantile (3) - Tetany

A 14 weeks old infant was admitted to the intensive care unit with life-threatening hypocalcemic-hyperphosphatemic spasms.

Hypocalcemia-hyperphosphatemia was found to have been caused by feeding a high phosphate/ low calcium soy milk.

The parents strongly believed that soy milk formulas were equivalent to breast milk and cow's milk formulas and lived on a strictly vegetarian diet. Therapy with calcium (at an initial dose of 2.25 mmol/kg/day) and 1.25 OH vitamin D3 (Rocaltrol, 0.25 microgram/day) normalized Ca, PO4, vitamin D and parathyroid hormone levels rapidly. Vegetarian feeding had led to life-threatening hypocalcemic hyperphosphatemic spasms in the infant.

Malnutrition and false nutritional beliefs have to be included as a potential cause of early hypocalcemia in infants.

Anil M et al., Hypocalcemic tetany in 'alternative' soy milk nutrition in the first months of life. Klin Padiatr, 208(6):323-6 1996 Nov-Dec.

Muscle (Spasm)

Muscle

Muscle rigidity and spasms occur with neurological disease and may contribute to contractures and shortening of muscle fibers that can interfere with motor behaviors, such as ambulation, or activities of daily living, such as combing hair, feeding or dressing.
The neuromuscular technique (NMT) and muscle energy technique (MET) are nursing interventions that can reduce pain and muscle rigidity, lengthen muscle fibers and increase range of motion necessary for normal motor behavior.

With some neurological diseases, muscle rigidity, increased muscle tone and muscle spasms reduce the range of motion of joints and the quality of movement. These changes often lead to contractures and impairments in performing daily tasks or ambulating, and thus, to loss of independence.

Soft tissue manipulation can be used to reduce muscle tension and spasms, lower pain and enhance the range of motion of joints dependent on the muscles involved.

Roberts BL: Soft tissue manipulation: neuromuscular and muscle energy techniques. J Neurosci Nurs, 29(2):123-7 1997 Apr.

Smoking (Spasm)

Smoking

Risk factors for pure coronary spasm are not known. Clinical observations have pointed to cigarette smoking, a known risk factor for obstructive coronary artery disease.

Studied premenopausal women, a population segment with the lowest prevalence of obstructive coronary artery disease. The cases were 21 premenopausal women (age range, 36-41 years) with angiographically proven coronary spasm.

[Coronary arteriograms.]

6 cases developed spontaneous coronary spasm before catheter engagement, and in 15, coronary spasm was induced by ergonovine provocation.

Only cigarette smoking was significantly more prevalent among coronary spasm cases. Cigarette smokers were 13 cases (62%) and 11 controls (17.5%) (p less than 0.001). The odds ratio was 7.7, with a 95% confidence interval of 2.6-23.1.

These findings suggest that there is a very strong association between cigarette smoking and pure coronary spasm in young women.

Caralis DG et al., Smoking is a risk factor for coronary spasm in young women. Circulation, 85(3):905-9 1992 Mar.

Vitamin B 6

Vitamin B 6

Vitamin B-6 is an important coenzyme in the biosynthesis of the neurotransmitters GABA, dopamine and serotonin and is therefore required for the normal perinatal development of the central nervous system.

In rat studies, biochemical and morphological abnormalities (decreased dendritic arborization and reduced numbers of myelinated axons and synapses) in the brains of pups from vitamin B-6 deficient dams were associated with behavioral changes such as epileptiform seizures and movement disorders.

In severely vitamin B-6 deficient human infants, similar behavioral abnormalities have been described. Marginally deficient neonates were found to have a lower birthweight and to display less mature reactive and adaptive behavior in the Brazleton Neonatal Assessment Scale than well-fed infants.

While it is not yet possible to define the exact amount of vitamin B-6 required to support optimal brain development, pregnant and lactating women should be encouraged to consume a diet that is rich in vitamin B-6.

Gerster H: The importance of vitamin "B 6" for development of the infant. Human medical and animal experiment studies. Z Ernahrungswiss, 35(4):309-17,1996.

 


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