Dysarthric Bengali speech: a neurolinguistic study.

BACKGROUND AND AIMS: Dysarthria affects linguistic domains such as respiration, phonation, articulation, resonance and prosody due to upper motor neuron, lower motor neuron, cerebellar or extrapyramidal tract lesions. Although Bengali is one of the major languages globally, dysarthric Bengali speech has not been subjected to neurolinguistic analysis. We attempted such an analysis with the goal of identifying the speech defects in native Bengali speakers in various types of dysarthria encountered in neurological disorders. SETTINGS AND DESIGN: A cross-sectional observational study was conducted with 66 dysarthric subjects, predominantly middle-aged males, attending the Neuromedicine OPD of a tertiary care teaching hospital in Kolkata. MATERIALS AND METHODS: After neurological examination, an instrument comprising commonly used Bengali words and a text block covering all Bengali vowels and consonants were used to carry out perceptual analysis of dysarthric speech. From recorded speech, 24 parameters pertaining to five linguistic domains were assessed. The Kruskal-Wallis analysis of variance, Chi-square test and Fisher's exact test were used for analysis. RESULTS: The dysarthria types were spastic (15 subjects), flaccid (10), mixed (12), hypokinetic (12), hyperkinetic (9) and ataxic (8). Of the 24 parameters assessed, 15 were found to occur in one or more types with a prevalence of at least 25%. Imprecise consonant was the most frequently occurring defect in most dysarthrias. The spectrum of defects in each type was identified. Some parameters were capable of distinguishing between types. CONCLUSIONS: This perceptual analysis has defined linguistic defects likely to be encountered in dysarthric Bengali speech in neurological disorders. The speech distortion can be described and distinguished by a limited number of parameters. This may be of importance to the speech therapist and neurologist in planning rehabilitation and further management.

Hepatopulmonory syndrome--an uncommon and severe complication of certain liver diseases.

Hepatopulmonary syndrome (HPS) is charaterised by arterial hypoxaemia found mainly in association with chronic liver disease (most commonly cirrhosis of liver) but also rarely with acute liver diseases like fulminant hepatic failure or Budd-Chiari syndrome. The purpose of this article is to present an uncommon but grave complication mostly associated with cirrhosis of liver and to differentiate this entry from cyanotic heart diseases or certain lung conditions. Investigations include history and physical examination, certain biochemical tests, upper gastro-intestinal (GI) endoscopy, abdominal ultrasonography, liver biopsy and venacavography in appropriate cases. Finally, the suspected cases underwent arterial blood gas (ABG) analysis and contrast enhanced echocardiography (CEE) for confirmation of the diagnosis of HPS. Of the 123 cases of cirrhosis of liver, three cases of HPS (2.4%) were found-all of them being males. Also one male patient with inferior vena cava (IVC) obstruction amongst other causes presenting with HPS was encountered. As of now, no medical treatment has been proved to be useful and liver transplant remains the only hope for this disorder.

Leptospirosis and Weil's disease in eastern India.

Leptospirosis is characterised by a broad spectrum of clinical manifestations varying from inapparent infection to fulminant fatal disease. Severe leptospirosis characterised by profound jaundice is referred to as Weil's disease. In the present study 20 patients of leptospirosis, of which 7 belonged to Weil's disease, were diagnosed based on the demonstration of IgM antileptospira antibody and supported by clinical correlation and appropriate biochemical markers. Overall, the male and female ratio was 17:3 and the same ratio for the Weil's disease was 6:1. The most common presentation involved fever, malaise and myalgia. Conjunctival congestion was found in 75% of the cases and jaundice was encountered in 90% of the cases. The prognosis of all these patients, including that of Weil's disease was excellent. Early recognition and initiation of antibiotic therapy were found to be important.

Expression of 5-amino levulinic acid induced photodynamic damage to the thylakoid membranes in dark sensitized by brief pre-illumination.

The 5-amino levulinic acid treated cucumber (Cucumis sativus L., CV. Pointsette) plants upon exposure to light (~ 30,000 lux) wilted within 6 h and died after 36 h due to photodynamic reactions. Thylakoid membranes, the site of accumulation of porphyrins, were damaged due to photodynamic reactions leading to the inhibition of membrane linked functions of photosystem II, photosystem I and the whole chain electron transport. Photosystem II was more susceptible to photodynamic damage than photosystem I. The exogenous electron donors Mn2+, diphenyl carbazide and NH2OH failed to donate electrons to photosystem II suggesting that the damage has taken place close to P680. The 5-amino levulinic acid treated plants exposed to 30 min of light did not show any damage to the thylakoid membranes. However, when the above plants were transferred to dark for 12 h there was substantial damage to the thylakoid membrane system.