Non-recurrent inferior laryngeal nerve

Surgical damage to the inferior laryngeal nerve is one of the most feared complications of thyroid surgery. Prevention of surgical injuries requires systematic, early exposure of the inferior laryngeal nerve. A detailed knowledge of anatomical variations is necessary. Non-recurrent inferior laryngeal nerve is a rare anomaly on the right side and is exceptional on the left. Whereas the typical course of the inferior laryngeal nerve is due to the embryological development of the aortic arch and supra-aortic vessels, non-recurrence is associated with a vascular anomaly such as a right retro-oesophageal subclavian artery. The nervous anomaly on the left side is possible only with the occurrence of cardiac dextroposition (situs viscerum inversus) and a left retro-oesophageal subclavian artery. The situation is more dangerous when a non-recurrent branch of the inferior laryngeal nerve is associated with a recurrent branch. This anomaly does not appear to be associated with a vascular anomaly in all cases. The authors describe three cases of right non-recurrent inferior laryngeal nerve observed and one recent case of combined non-recurrent and recurrent nerve, highlighting the anatomical and surgical features of this anomaly.     

Resting energy expenditure in diabetic and nondiabetic patients with liver cirrhosis: relation with insulin sensitivity and effect of liver transplantation and immunosuppressive therapy

BACKGROUND: Hypermetabolism, insulin resistance, and diabetes are common in patients with liver cirrhosis. OBJECTIVE: We assessed whether diabetes and insulin resistance influence postabsorptive energy homeostasis in these patients and whether liver transplantation (LTx) and immunosuppressive drugs affect these relations. DESIGN: Twenty-six patients with liver cirrhosis (16 with and 10 without diabetes) were studied with an insulin clamp and indirect calorimetry. Eleven of these subjects were studied 9 mo after LTx to longitudinally assess its effects. To cross-sectionally explore a longer follow-up period, we studied 65 patients 6, 14, and 32 mo after LTx. Seven patients with chronic uveitis (receiving immunosuppressive therapy) and 20 healthy subjects served as control subjects. RESULTS: Diabetic and nondiabetic patients with cirrhosis had insulin resistance (S(I(clamp)); P < 0.03) and higher measured resting energy expenditure (REE) as a percentage of predicted REE than did healthy subjects (107.6 +/- 1.8% compared with 97.4 +/- 2.3%; P < 0.03), and these 2 alterations were associated (R(2) = 0.119, P = 0.0002). The longitudinal study showed an improvement in the 2 variables after LTx, but full restoration was not achieved. The cross-sectional analysis confirmed this observation in patients studied 6 mo (n = 28) after LTx. In patients studied 14 (n = 21) and 32 mo (n = 16) after LTx, S(I(clamp)) and measured REE as a percentage of predicted REE were not significantly different from those in control subjects. CONCLUSIONS: In patients with liver cirrhosis, higher-than-normal postabsorptive REE was associated with insulin resistance regardless of diabetes. This abnormality persisted in patients studied 6-9 mo after LTx but improved simultaneously with the improvement in insulin sensitivity thereafter.     

Investigation into the role of apolipoprotein B gene 8344C/T variant on plasma cholesterol levels by allele-specific PCR amplification

The 8344C/T polymorphism of the apoB gene was genotyped by an original modification of PCR allele-specific amplification consisting in a single amplification reaction double-primed by two opposite allele-specific oligonucleotides nested in a larger amplified fragment. This method was used to genotype 200 randomly selected healthy individuals (113 males, 87 females). The frequency of the rare allele in this random Italian population was 0.240, i.e. not far from the 0.282 frequency observed in hypocholesterolemic Norwegians and suggestive of a moderating effect on LDL levels of our population. However, we did not find any significant cholesterol-lowering effect of this polymorphism either by comparing the frequency of mutant alleles in the population stratified for its plasma lipoprotein levels or by studying the association between ApoB genotype and the different lipoproteins. In conclusion this ApoB polymorphism appeared to have a secondary role in LDL- and HDL-cholesterol variations of our population.     

Oral cancers and the need for secondary prevention programs

Each year, 250,000 people all over the world develop oral cancer, while 130,000 die for this condition. In Italy, these figures are 6000 and 3000, respectively. The 53% average survival rate in five years is one of the lowest, although it increases to 72-86% if oral cancer is diagnosed at the TNM stage I. However, in more than half the cases this condition is diagnosed at more severe stages. This situation can improve significantly because the oral cavity can be easily checked and the cancer is often predictable by precancerous lesions. Since alcohol and tobacco are responsible for 75% of cases, primary prevention basically relies on their control. Secondary prevention, aimed at the early detection of this condition, is based on the examination of oral mucosae and can be performed by dentists, dental hygienists or the patients themselves. The first step to take is to foster information among the subjects at risk, namely people over 40. The authors suggest that educational programs should be held by health professionals so as to teach patients how to perform selfexamination and address to hospitals in case of suspected cancerous lesions.     

p38 MAP kinase mediates the cell death induced by PrP106-126 in the SH-SY5Y neuroblastoma cells

Prion diseases are neurodegenerative pathologies characterized by the accumulation in the brain of a protease-resistant form of the prion protein (PrP(c)), named PrP(Sc). A synthetic peptide homologous to residues 106-126 of PrP (PrP106-126) maintains many PrP(Sc) characteristics. We investigated the intracellular signaling responsible for the PrP106-126-dependent cell death of SH-SY5Y, a cell line derived from a human neuroblastoma. In this cell line, PrP106-126 induced apoptotic cell death and caused activation of caspase-3, although the blockade of this enzyme did not inhibit cell death. The p38 MAP kinase blockers, SB203580 and PD169316, prevented the apoptotic cell death evoked by PrP106-126 and Western blot analysis revealed that the exposure of the cells to the peptide induced p38 phosphorylation. Taken together, our data suggest that the p38 MAP kinase pathway can mediate the SH-SY5Y cell death induced by PrP106-126.     

Dystrophin stabilizes alpha 3- but not alpha 7-containing nicotinic acetylcholine receptor subtypes at the postsynaptic apparatus in the mouse superior cervical ganglion

The nicotinic acetylcholine receptor (nAChR) subtypes were characterized in the superior cervical ganglion (SCG) of wild-type and dystrophin-lacking mdx mice. The binding of Epibatidine and alphaBungarotoxin, ligands for alpha3- and alpha7-containing receptors, respectively, revealed, for each ligand, a single class of high-affinity binding sites, with similar affinity in both wild-type and mdx mice. The Epibatidine-labeled receptors were immunoprecipitated by antibodies against the alpha3, beta2, and beta4 subunits. Immunocytochemistry showed that the percentage of alpha3-, beta2-, and beta4- but not of alpha7-immunopositive postsynaptic specializations was significantly lower in mdx than in wild-type mouse SCG. These observations suggest that the mouse SCG contains nAChRs, stabilized by dystrophin, in which the alpha3 subunit is associated with the beta2 and/or beta4 subunits. Conversely, dystrophin is not involved in the stabilization of the alpha7-containing nAChRs, as the percentage of alpha7-immunopositive synapses is similar in both wild-type and mdx mouse SCG.     

Polysomnographic study of sleeplessness and oneiricisms in the alcohol withdrawal syndrome

We describe a polysomnographic observation of the acute phase of the alcohol withdrawal syndrome, characterized by an alteration of the sleep-wake cycle and by the absence of non-rapid eye movement sleep. An atypical transitional state between rapid eye movement sleep and wake with hallucinations and enacting-dream behaviors represented the sole sleep pattern. Analogies of alcohol withdrawal syndrome with fatal familial insomnia and Morvan's fibrillary chorea suggest a common pathophysiological mechanism in these conditions.     

Magnetization transfer can predict clinical evolution in patients with multiple sclerosis

The clinical course of multiple sclerosis (MS) is highly variable ranging from benign to aggressive, and is difficult to predict. Since magnetization transfer (MT) imaging can detect focal abnormalities in normal-appearing white matter (NAWM) before the appearance of lesions on conventional MRI, we hypothesized that changes in MT might be able to predict the clinical evolution of MS. We assessed MR data from MS patients who were subsequently followed clinically for 5 years. We computed the mean MT ratio (MTr) in gray matter, in lesions identified on T2-weighted MRI, and in NAWM, as well as in a thick central brain slice for each patient. Patients were divided into stable and worsening groups according to their change in Expanded Disability Status Scale (EDSS) scores over 5 years. We calculated the sensitivity, specificity, predictive value, and odds ratio of the baseline MTr measures in order to assess their prognostic utility. We found significant differences in baseline MTr values in NAWM (p = 0.005) and brain slice (p = 0.03) between clinically stable and worsening MS patients. When these MTr values were compared with changes in EDSS over 5 years, a strong correlation was found between the EDSS changes and MTr values in both NAWM (SRCC = −0.76, p < 0.001) and in the brain slice (SRCC = 0.59, p = 0.01). Baseline NAWM MTr correctly predicted clinical evolution in 15/18 patients (1 false positive and 2 false negatives), yielding a positive predictive value of 77.78 %, a negative predictive value of 88.89 %, and an odds ratio of 28. The relationship between 5-year changes in EDSS and MTr values in T2 weighted MRI lesions was weaker (SRCC = −0.43, p = 0.07). Our data support the notion that the quantification of MTr in the NAWM can predict the clinical evolution of MS. Lower MTr values predict poorer long-term clinical outcome. Abnormalities of MTr values in the NAWM are more relevant to the development of future patient disability than those in the T2-weighted MRI lesions. Received: 3 May 2001, Received in revised form: 11 October 2001, Accepted: 22 October 2001     

MR correlates of cerebral atrophy in patients with multiple sclerosis

Objective To investigate the in-vivo correlates of brain atrophy in patients with multiple sclerosis (MS) by assessing the relationship between normalized measures of brain volume (NBV) and other magnetic resonance (MR) measures of tissue damage. Background Brain atrophy diffusely occurs and progressively increases in patients with MS. Nevertheless, the mechanisms leading to brain atrophy in this disease are not fully understood. Methods MR examinations were performed in 20 patients with relapsing-remitting MS. Conventional MRI was used to assess NBV and total brain T2-hyperintense and T1-hypointense lesion volumes. Proton MR spectroscopic imaging and diffusion tensor MR imaging were also performed for large portions of brain containing mainly normal-appearing tissue to provide indices of tissue damage, including N-acetylaspartate to creatine ratio (NAA/Cr) and mean diffusivity (). Results Values of NBV correlated significantly with those of average brain (r = -0.58, p = 0.007) and NAA/Cr (r = 0.67, p < 0.001). The relationship of these markers of tissue damage to NBV was also found when NAA/Cr and were computed together in a composite MR score (r = 0.70, p < 0.001). In contrast, NBV values did not correlate with measurements of average lesion , T₂ and T₁ weighted total brain MRI lesion volumes. Conclusions This study suggests that brain atrophy in MS is not simply due to axonal loss, but rather reflects a more generalized process that involves various brain tissue components. Damage to the normal-appearing tissue rather than the extent and intrinsic pathology of macroscopic lesions seems to be important in the destructive process leading to MS-related irreversible cerebral atrophy. Received: 13 September 2001 Received in revised form: 18 January 2002 Accepted: 4 March 2002