Should amiodarone be discontinued before cardiac surgery?

Between October 1985 and October 1986, 37 patients, chronically treated with amiodarone, underwent general anesthesia for cardiac, thoracic or vascular surgery. Among them, the 8 non-cardiac surgery patients showed neither intra-, nor postoperative complications. The 29 cardiac surgery patients, had various complications ranging from dysrhythmias (52%), sometimes necessitating a pacemaker (24%), to marked and even fatal vasoplegia. We describe the only fatal case and compare our complication rate with that described in the available literature. Most complications could be symptomatically treated. In addition, amiodarone has a very long elimination half-life: therefore withdrawal before surgery implies delaying operations by several weeks, and puts patients at increased risk of malignant dysrhythmias. However, fatal vasoplegia does occur, and its real incidence should be assessed by a broader survey.     

Release of monoamines from striatal slices by phenelzine and β-phenylethylamine

1. 1. Slices of striatum obtained from control rats were incubated with H-serotonin (³H-5HT) or ¹⁴C-dopamine (¹⁴C-DA) in the presence of pargyline; then, they were subjected to a rapid transfer technique during which they were washed either with a normal Krebs buffer or one containing known quantities of phenelzine (PEH) or β-phenylethylamine (PE).

2. 2. Both PEH and PE were able to stimulate releases of ³H-5HT and ¹⁴C-DA that were greater than control. More ¹⁴C-DA than ³H-5HT was released by both compounds. Much lower concentrations of PE than of PEH were required to stimulate monoamine release.

3. 3. Other rats were Injected intraperitoneally with behaviourally effective doses of either PEH or PE and were killed at various times.

4. 4. The concentrations of PEH or of PE in the striata of these animals were very high 15 min after I.P. Injection, but declined rapidly thereafter.

5. 5. These results may be Interpreted to suggest that after I.P. Injection, sufficient levels of PEH and PE were attained in the rat striatum to stimulate release of endogenous 5HT and DA.

Idiopathic infantile arterial calcification with cardiac,renal and central nervous system involvement

Idiopathic infantile arterial calcification was diagnosed in a 2 week old infant with failure to thrive associated with neurological, renal and cardiac signs. Therapy with diphosphonate resulted in a complete resolution of vascular calcifications. At the age of 2 years the child is doing well but requires medical treatment for arterial hypertension.     

SPECT regional cerebral blood flow alterations in naltrexone-precipitated withdrawal from buprenorphine

The effects of naltrexone-precipitated withdrawal from buprenorphine on behavior and regional cerebral blood flow (rCBF) were studied in 11 opiate-dependent patients. Patients initially received buprenorphine, 2 mg sublingually, every day for 7 days. They were then challenged sequentially with placebo and naltrexone, 25 mg orally, before single photon emission computed tomography with technetium-⁹⁹m-d,l-hexamethyl-propylene amine oxime as tracer. Behavioral ratings of withdrawal severity were made before and after naltrexone/placebo administration. Naltrexone produced significantly greater signs and symptoms of opiate withdrawal than placebo. Analysis of variance revealed no significant regionally specific effect of naltrexone on rCBF ratios. Severity of withdrawal, however, showed a significant negative correlation with rCBF in the anterior cingulate cortex following naltrexone. These results are interesting as the anterior cingulate region has been implicated in the emotional component of pain and in opiate-induced analgesia.     

Increase in albumin, IgG, and IgM blood-nerve barrier indices in human diabetic neuropathy.

The albumin (Alb), IgG, and IgM concentrations in the endoneurium of fascicular sural nerve biopsy samples were evaluated in controls (n = 9 or 10), diabetic patients without neuropathy (n = 6), and diabetic patients with polyneuropathy (n = 17 or 18). These values were significantly increased in diabetic patients with and without neuropathy when expressed both per endoneurial dry weight or endoneurial total protein compared to biopsy samples from healthy controls. When these concentrations, expressed per endoneurial total protein, were related to plasma concentrations similarly expressed, the resulting blood-nerve barrier (BNB) indices were significantly increased for Alb (6.1 times; P less than 0.00001), IgG (4.9 times; P = 0.00037), and IgM (2.7 times; P = 0.015). The diabetic patients without neuropathy (defined as having an index of pathology of greater than 0.65; a measure of the severity of the pathological abnormality based on morphological criteria) also had significant increases in two of these BNB indices that were intermediate between the diabetic neuropathy patients and controls (Alb, 3.9 times controls; P = 0.00002: IgG, 4.6 times controls; P = 0.00016: IgM, 1.8 times controls; not significant). No correlations were observed between the endoneurial concentrations of these plasma proteins or the BNB indices and the index of pathology, suggesting that these increases in endoneurial plasma proteins precede the pathologic alterations. The increased values for the diabetics in the absence of pathological abnormalities may prove useful in predicting neuropathic complications. The ratio of the IgG-BNB index to the Alb-BNB index was decreased 19%, and the ratio of the IgM-BNB index to the Alb-BNB index was decreased 56% in diabetic neuropathy patients compared to controls. Although the IgG and IgM concentrations are increased in the diabetic endoneurium, the Alb increase is greater and a mechanism other than size indiscriminate extravasation of plasma proteins, therefore, is suggested. Morphometric assessment of the endoneurial compartments, which would be expected to contain these plasma proteins, suggests that they are not altered in diabetic neuropathy; hence, it is hypothesized that the observed increase in endoneurial concentration of these plasma proteins results from altered transport through the endothelial or perineurial barrier, which supports an underlying vascular mechanism in the development of diabetic polyneuropathy.     

Hereditary motor and sensory neuropathy with diaphragm and vocal cord paresis

We describe two kindreds with an autosomal dominant inherited disorder characterized by a variable degree of muscle weakness of limbs, vocal cords, and intercostal muscles and by asymptomatic sensory loss, beginning in infancy or childhood in severely affected persons. Life expectancy in severely affected patients is shortened because of respiratory failure. Because nerve conduction velocities are normal and it is an inherited axonal neuropathy, we classify the disorder as a variety of hereditary motor and sensory neuropathy type II (HMSN II) (HMSN IIc). The present report provides further evidence for heterogeneity among the hereditary motor and sensory neuropathy type II disorders. In one large pedigree with the type IIc disorder, no linkage to DNA markers known to map near the HMSN IA locus on chromosome 17p or the HMSN IB locus on chromosome 1q was demonstrated.     

Continuous monitoring of panic

Data on naturally occurring panic attacks were gathered through continuous self-monitoring for 94 patients suffering from panic disorder with agoraphobia. A total of 1276 panic attacks were collected. In this article various aspects of panic attacks, including severity, duration and time of onset and situations in which panic occurs are addressed. In addition, the symptoms of panic were investigated, examining the (in)variability of attacks within each patient and the patterning of symptoms in the entire group of patients. The most important findings were as follows: attacks occurred predominantly in nonphobic situations; nocturnal panic attacks were generally more severe than attacks during the day; symptom patterns across various attacks, stemming from the same patient, were rather variable; and finally, a substantial number of the attacks (40%) did not meet the DSM-III-R criteria for number of symptoms.     

Lumbar nerve root: the enigmatic eponyms

Man's quest for recognition has not escaped the physician, whose contributions to medicine perpetuate his name in print. It is a final grasp for professional immortality, which for men like Imhotep and Hippocrates, has prevailed for millennia. This fervor was particularly evident in the latter 19th century, which created a flurry of eponyms, often two or more physicians publishing the same clinical observation. This article reviews the eponym epidemic as it relates to lumbar radiculopathy.     

Polyglucosan body axonal enlargement increases myelin spiral length but not lamellar number

The area of the unrolled myelin sheet of internodes of myelinated fibers (MF) of peripheral nerve is thought to be determined by axonal caliber and internodal length. We studied the effect of a focal increase of axonal caliber due to the deposition of polyglucosan bodies (PGB), amylopectin-like glucose polymers, on number of myelin lamellae (NL), interlamellar distance (periodicity), and myelin spiral length (MSL) from a sural nerve biopsy specimen of a patient with chronic inflammatory demyelinating polyneuropathy. Axonal area, NL, periodicity, and MSL were estimated within internodes of MF above, at, and below PGB. The axon caliber at the level of the PGB was significantly (P less than 0.002) increased when the PGB was included. At the PGB, NL and their periodicity were not significantly different from those above or below the PGB. The MSL was significantly longer overlying the PGB than it was in the same internode above or below the PGB. Because slippage or stretching of the myelin sheath as well as movement of molecular constituents of myelin is not likely over large distances, localized biosynthesis and assembly of new myelin may explain this increase of MSL.