Cerebellar abscess and syringomyelia due to isoniazid-resistant Mycobacterium tuberculosis.

A 19-year-old immunocompetent man was admitted to hospital with diplopia, nausea, vomiting and change in mental status. The patient had a history of tuberculous meningitis that was diagnosed at another hospital 6 months before the present admission, and at that time anti-tuberculosis treatment was initiated using a first-line drug combination. A computed tomography (CT) scan of the brain revealed non-communicating hydrocephalus. A ventriculo-peritoneal shunt was inserted surgically. Two months later, the patient was hospitalized again for fever, dysphagia and left hemiparesis. At that time, his cranial CT findings were within normal limits; however, magnetic resonance imaging (MRI) revealed an irregular multilocular peripheral contrast-enhancing lesion in the posterior fossa. The abscess was surgically drained. The presence of acid-fast bacilli in the abscess material was demonstrated by Ziehl-Neelsen staining. Mycobacterium tuberculosis grew on Lowenstein-Jensen culture medium, and the strain was found to be resistant to isoniazid. One month after the operation, the patient became quadriparetic. Cervical MRI revealed a cervico-thoracic syringomyelitic cavity, after which a syringoperitoneal shunt was placed. Treatment with four drugs was continued for 10 months, and then treatment with three drugs for a total period of 18 months. The patient recovered, with residual quadriparesis. Even though very rare, isoniazid-resistant M. tuberculosis may be the causative agent of progressive tuberculosis.     

Clinical utility of dorsal sural nerve conduction studies in healthy and diabetic children.

OBJECTIVE: Monitoring of the dorsal sural sensory nerve action potential (SNAP) is a sensitive method for detection of peripheral neuropathies. We tried to determine the normal dorsal sural nerve conduction values of the childhood population and assessed the clinical utility of this method in diabetic children who have no clinical sign of peripheral neuropathy. METHODS: In the study, 36 healthy and 27 diabetic children were included. In all subjects peripheral motor and sensory nerve studies were performed on the upper and lower limbs including dorsal sural nerve conduction studies. RESULTS: The dorsal sural SNAP mean amplitude was 8.24+/-3.08 microV, mean latency was 2.47+/-0.48 ms, mean sensory conduction velocity was 41.63+/-5.43 m/s in healthy children. Dorsal sural SNAPs were absent bilaterally in one diabetic patient. In the other 26 diabetic patients, the mean dorsal sural nerve distal latency was longer (2.93+/-0.63 ms, P = 0.004), mean SCV was slower than in healthy subjects (36.68+/-7.66 m/s, P = 0.005). However, dorsal sural nerve amplitude was not different between the groups. A dorsal sural nerve latency of more than 2.9 ms had a sensitivity of 50% and a specificity of 75%. A dorsal sural nerve velocity of less than 36 m/s had a sensitivity of 54% and a specificity of 92%. CONCLUSIONS: We designated the reference values of the dorsal sural nerve in healthy children. In addition, our findings suggest that dorsal sural nerve conduction studies may have value to determine neuropathy in the early stages in children with diabetes. SIGNIFICANCE: The dorsal sural nerve conduction studies in diabetic children may have value to determine the neuropathy in its early stages.     

Dydrogesterone-induced hepatitis and autoimmune hemolytic anemia.

Dydrogesterone, similar to women's natural progesterone, has been used in a wide range of gynecological conditions. Despite its widespread use, dydrogesterone-induced hepatotoxicity and dydrogesterone-induced hemolytic anemia have, to the best of our knowledge, never been reported previously. We describe a case of hepatitis and warm antibody hemolytic anemia due to dydrogesterone.     

Using diazepam and atropine before strabismus surgery to prevent postoperative nausea and vomiting: a randomized, controlled study.

OBJECTIVE: To evaluate the efficacy of diazepam and atropine sulfate premedication in preventing nausea and vomiting after strabismus surgery under general anesthesia. METHODS: Fifty children age 4 to 15 years who underwent strabismus surgery at Cukurova University Medical Faculty, Department of Ophthalmology, from February 2000 to June 2000 were randomized into 2 groups: 25 children in the control group did not receive premedication, whereas 25 children in the treatment group received premedication with 0.15 mg/kg diazepam and 0.015 mg/kg atropine sulfate. Occurrence of postoperative nausea and vomiting (PONV) was recorded. RESULTS: The incidence of PONV was lower in the premedicated group (P <.018, chi(2) test). CONCLUSIONS: It is concluded that diazepam and atropine sulfate premedication decreases nausea and vomiting after strabismus surgery.     

A second locus (GLC3B) for primary congenital glaucoma (Buphthalmos) maps to the 1p36 region

Primary congenital glaucoma (gene symbol: GLC3) is an ocular disorder that occurs for 0.01-0.04% of blind people. In the majority of familial cases reported so far, this condition is inherited as an autosomal recessive trait. We have recently used a group of 17 GLC3 families with a minimum of two affected offspring and consanguinity in most of the parental generation and mapped the first GLC3 locus (GLC3A) to the 2p21 region. Six families did not show any linkage to the GLC3A locus and thus provided evidence for genetic heterogeneity of this disorder. A total of eight families unlinked to the 2p21 region were used to search for the chromosomal location of the second GLC3 locus. Herein, we describe mapping of a new locus (designated GLC3B) for primary congenital glaucoma to the short arm of chromosome 1 (1p36.2-36.1) that is situated centromeric to the neuroblastoma and Charcot-Marie-Tooth type 2A (CMT2A) loci. A total of 17 DNA markers were genotyped from this region of chromosome 1. Four families showed no recombination with the two markers D1S2834 and D1S402 with a maximum lod score of 4.510 and 4.157 respectively. Pairwise and multipoint linkage analysis and inspection of the haplotypes revealed that the remaining four families are not linked to this part of chromosome 1, thus providing further evidence that at least one more locus for the autosomal recessive form of GLC3 must exist in the genome. Based on the recombination events, the overall linkage map of this region is: tel-D1S1192-D1S1635-D1S1193 - (D1S1597/-D1S489/D1S228)- [GLC3B/D1S2834/D1S402] - (D1S1176/D1S507/D1S407) - D1S2728-(MFAP2/D1S170) - D1S1368 - D1S436- D1S1592-cen.      

Motor neuron degeneration due to aluminium deposition in the spinal cord: a light microscopical study.

For a long time, aluminium has been considered as an indifferent element from a toxicological point of view. In recent years, it became clear that aluminium is a potential toxic agent in humans and has been implicated in the pathogenesis of several clinical disorders, such as dementia, respiratory tract disorders and allergic reactions. Chronic exposure to aluminium fumes, inhalation of aluminium and aluminium-oxide powder increase the risk to develop serious central nervous system pathology, in particular Alzheimer's disease and amyotrophic lateral sclerosis (ALS). In the present study, 3 experimental and 1 control group of rats were used to study the effects of aluminium on the central nervous system. Aluminium was injected intracisternally as a single dose (50 micrograms for group I, 100 micrograms for group II and 300 micrograms for group III) to the experimental groups (n = 5 in each group). The same dose was given at 3 months after the first injection to all groups. The control group (n = 5) was intracisternally given a physiological salt solution. Electromyography (EMG) was applied to the rats of the experimental groups. Rats were decapitated at 3 months after the second injections. Spinal cord samples from lumbar and cervical regions were removed and histological examination was performed. Light microscopical investigations revealed severe degeneration in motor neurons of the rats treated with 300 micrograms. Neurofibrillary tangle formation, chromatolysis and abnormal localization of the nuclei were found in swollen perikarya. Extreme loss of motor neurons with "ghost cell" appearance was found in that group. Sections of spinal cords of rats treated with lower doses of aluminium showed a moderate degree of motor neuron damage. EMGs of rats treated with the high dose of aluminium revealed severe acute denervation whereas treatment with lower doses resulted in moderate denervation. We conclude that aluminium may cause severe motor neuron damage in rat spinal cord resembling ALS.     

Contradictory effects of chlorpromazine on endothelial cells in a rat model of endotoxic shock in association with its actions on serum TNF-alpha levels and antioxidant enzyme activities.

We examined the effects of the phenothiazine derivative, chlorpromazine on thoracic aortic endothelial cell histology (14 h after LPS challenge) in a model of endotoxic shock in rats. Since excessive formation of tumor necrosis factor-alpha (TNF-alpha) and oxygen-derived free radicals contribute to endothelial injury in endotoxemia, we also evaluated the effect of the drug on the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase in liver tissue in this model and tried to find out whether this possible effect was associated with a change in serum TNF-alpha levels (measured 90 min after chlorpromazine administration). Endotoxemia was induced by a single i.p. injection of lipopolysaccharide (LPS) (5 mg kg(-1) in 1.5 ml of saline; LPS from Escherichia coli serotype 055:B5, L-2880, Sigma Chemical Company). Electron microscopic evaluation of the aortas revealed that chlorpromazine (administered 30 min prior to LPS challenge), in smaller doses (3 mg kg(-1)) ameliorated the endothelial cell injury caused by LPS, whereas it caused deterioration of endothelial cell morphology in higher doses (10 and 25 mg kg(-1)). Chlorpromazine administration caused a significant reduction in serum TNF-alpha levels, which was correlated well with an increase in SOD activity in all drug doses (3, 10 and 25 mg kg(-1)). Catalase activity was increased only in the 25 mg kg(-1) chlorpromazine group.