Postural control and central motor pathway involvement in type 2 diabetes mellitus: dynamic posturographic and electrophysiologic studies

Postural instability causes limitations in daily activities of diabetic patients. There is paucity of data regarding central motor pathway involvement in these patients and its relation to postural control. To evaluate postural control and central motor pathway involvement in type 2 diabetic patients. The study included 30 type 2 diabetic patients and 15 healthy, age and sex matched control subjects. Both groups were subjected to physical and full neurological examination, in addition to electrophysiological study including peripheral conduction study and MEPs recorded from the feet muscles. Total neuropathy score was calculated. In addition, dynamic posturographic tests were performed including sensory organization test and MCT. Most of the dynamic posturographic parameters were significantly impaired in diabetic patient group. There were significant abnormalities in most of the parameters of the peripheral conduction study of the patients compared to the controls. According to the Total neuropathy score, 20 patients had peripheral neuropathy. In addition, there was significant prolongation of the left CMCT, decreased left MEP amplitude and increased MEP resting motor threshold on both sides in the patients compared to the control group. Dynamic posturographic parameters showed correlation with most of the parameters of the peripheral conduction study and few of the MEP parameters. Logistic regression analysis showed peripheral neuropathy as the main factor implicated in postural instability in these patients. However, significant correlation was found between MEP amplitude and MCT composite score in patients without peripheral neuropathy. Although type 2 diabetic patients had prolonged CMCT, decreased amplitude and increased resting motor threshold of the MEP response, peripheral neuropathy was the main factor implicated in postural instability. However, the central motor pathway changes documented could be implicated as a possible cause

Distribution of cyclooxygenase-3 [COX-3] in rat nervous system

Cyclooxygenase-3 [Cox-3] is a recently identified cyclooxygenase which is inhibited by paracetamol related drugs rather than traditional non-steroidal anti-inflammatory. In this study the distribution of Cox-3 has been studied in the rat nervous system both in the central and peripheral nervous system. Ten adult male Wistar rats weighing 300-400 g were killed by decapitation under brief anesthesia. Nervous system; brains, spinal cords, spinal ganglia and spinal nerves were removed and processed for immunohistochemisty using an antibody raised against Cox-3. Cox-3 was widely distributed in the rat nervous system. The expression appeared mainly neuronal. In the central nervous system, Cox-3 was localized in neurons in the brain and spinal cord. In the brain Cox-3 was highly expressed in cerebral cortex, hippocampus and cerebellum. In the peripheral nervous system Cox-3 was localized in neurons in the spinal ganglia and in the spinal nerves. Cox-3 was widely distributed in the nervous system. Thus, this isoform could be contributing to the generation of the physiological levels of prostaglandins normally for needed for homeostatic regulation in the nervous system. Localisation of Cox-3 in areas associated with nociception and pain such as brain, spinal cord and spinal ganglia support the hypothesis that Cox-3 may be the central target of paracetamol and other related centrally acting analgesics/antipyretics

Impact of long-term oral iron supplementation in breast-fed infants.

OBJECTIVE: To weigh benefits of oral iron supplements on infant's growth against its potential hazards. METHODS: 248 exclusively breast-fed infants aged 4-6 months were consecutively enrolled and divided into treatment group given iron containing multivitamin (TG = 198) and control group (placebo, PG = 50) given the same multivitamin but without is subdivided according to clinical assessment into group A (well nourished) and group B (malnourished); both were further stratified according to basal blood iron status. Assessment was done after 6 and 12 months with concurrent collection of morbidity parameters (diarrhea and fever). Data were normalized and analyzed using SPSS and Eurogrowth softwares. RESULTS: After 6 months treatment, weight and length gain was better in TG compared to placebo especially evident in anemic malnourished infants (P 0.05). Morbidity risk was linked to immunologic background of infant; odds ratio for diarrhea and fever was higher in malnourished compared to well nourished (P 0.05) or iron therapy (P for well-nourished non-anemic treatment vs PG > 0.05). CONCLUSION: Oral iron supplementation resulted in better effects on growth velocity of breast fed infants especially those who were initially malnourished and anemic or at least iron depleted, with less marked morbidity than in iron replete infants.

Maternal serum thyroid hormones in severe preeclamptic patients

There are controversies about the concentration of thyroid hormones in preeclamptic patients and its clinical significance. To study the thyroid hormones levels in severe preeclamptic This study included 63 pregnant women [31 with severe preeclampsia and 32 healthy normotensive controls]. Patients were stratified according to gestational age. Free T3 [triiodothyronine] free T4 [thyroxin] and TSH [thyroid stimulating hormone] were measured using radioimmunoassay. Mean TSH is significantly increased in preeclamptic patients as compared to control subjects' while FT4, FT3 were comparable in both groups. TSH levels were not correlated to gestational age or severity of preeclampsia. Mean serum TSH levels were significantly increased without concomitant changes in FT4, FT3 in severe preeclampsia compared to normal pregnancy and this hormonal change was not related to gestational age or degree of severity of preeclampsia. The values of those findings are not clear. However, abnormal TSH titer might be associated with a risk for occurrence of preeclampsia, so studying TSH levels in high risk women form early pregnancy might be of value in the prediction of preeclampsia

Maternal mortality in Kasr EL Aini Hospital: Eleven years experience

To estimate the maternal mortality rate in Kasr AL Aini hospital, Cairo University, Egypt over eleven years duration to suggest different strategies to maternal mortality. Materials and Retrospective analysis of the mortality the period between 1992 to 2003. WE divide the duration of study into three periods as prophylactic were started in the second period and continued during the third period. The number of maternal deaths in the 1st period [1992-1995] was 61 with maternal mortality ratio [MMR] of 207 per 100,000 live births, while in the 2nd period [1997-2000] the number of maternal deaths was 43 with MMR of 118. Finally in the 3rd period [2001-2003] the number of maternal deaths was 37 with MMR of 97.1. Comparison between maternal mortality in 1st period and 3rd period was statistically significant. Relative risk was 2.39 [95% CI 1.56-3.71] [p = 0.000015]. The main causes of maternal mortality were postpartum hemorrhage, complications of sever hypertensive disorders, anesthetic complications and rheumatic heart diseases. Maternal deaths occurred in most of cases in late pregnancy and labor mostly due to postpartum hemorrhage and sever hypertensive disorders during pregnancy. Maternal mortality involves complex mixture clinical, infrastructural and social causes and requires a multifaceted approach, however it can effectively avoided and prevented through improving antenatal care, emergency obstetric services and reform of internship training program.

Histological changes of the brain tissue in pilocarpine epileptic experimental model before and after the use of antiepileptic and antioxidant substances

Epilepsy is a chronic, dynamic neurological disorder associated with ongoing neuronal damage, particularly when uncontrolled. Systemic administration of pilocarpine to rats results in generalized tonic clonic seizures and subsequent neurodegeneration similar to that observed in certain types of human epilepsy. Brain damage is supposed to be secondary to free radical production, thus raising the theory of the use of antioxidants as neuroprotective substances. To throw light on the evidence for the role of oxidative injury in epilepsy, the brain damaging action of the antiepileptic drugs and the rationale for use of antioxidant therapy in epilepsy. Eighty adult albino rats were divided into 4 groups; group I served as a control, group II were injected with pilocarpine hydrochloride intraperitoneal for induction of seizures, group III were given phenytoin [antiepileptic drug] before pilocarpine injection, while group IV were given vitamin C before being injected with pilocarpine. The animals were observed for the frequency of fits and mortality rate. The brain tissue of the sacrificed rats were processed for both light microscopical and ultrastructural study. Animals that possessed seizures following pilocarpine injection showed increased vascularisation, neuronal loss, gliosis, and silver stained proliferated dendrites by light microscope. Ultrastructural study revealed nuclear and cytoplasmic vacuolization, and destruction of mitochondria. Animals treated with phenytoin although showed reduction of the number of convulsing animals and mortality rate, yet all pathological findings found in pilocarpine group were observed. Instead the use of vitamin C showed a significant protective effect on the brain tissue. Although there is a documented brain damage of epileptic seizures and also antiepileptic drugs, antioxidants have a protective action against these brain damaging effects

Anatomical variations of the palmar cutaneous branch of the median nerve

Twenty cadaveric upper limbs were studied to identify the course of the palmar cutaneous branch of the median nerve [PCBMN] and its relation to the commonly used surgical landmarks of the palm of the hand. Dissection was begun in the forearm by exposing the median nerve, then the incision was extended distally into the palm along the thenar crease. The PCBMN was then exposed at the radial side of the median nerve and traced distally into the palm. The relationship of the PCBMN to the overlying soft tissue landmarks was then measured at the level of the distal wrist crease. The palmar cutaneous nerve of the median nerve was found closely underlie the thenar skin crease [range of 6 mm ulnar to 6 mm radial to the thenar skin crease]. The nerve traveled an average of 5 mm radial to the interthenar depression [range, 0- 12 mm redial]. So, these anatomical variations should be recommended for surgical approaches to the carpal tunnel release