Musculoskeletal Pain after Stroke: Prevalence, patterns and distribution among survivors in Maiduguri, North Eastern Nigeria

Background: Musculoskeletal pain is one of the factors that limit movements at a joint and impede functional use of the limb as well as rehabilitation activities after stroke. Objective: This study determined the prevalence, pattern and distribution of musculoskeletal pain among stroke survivors receiving physiotherapy care in Maiduguri. Methods: A cross-sectional study design was used to recruit 94 stroke survivors from the physiotherapy clinics of two randomly selected tertiary hospitals in Maiduguri. In addition to sociodemographic and clinical characteristic information, musculoskeletal pain was assessed with the Box-Numerical Rating Scale. Prevalence, pattern and distribution of musculoskeletal pain were computed with frequency and percentages. Chi-square test was employed to compare the difference in the prevalence of musculoskeletal pain among participants with various socio-demographic and clinical characteristics. Results: The mean age, post-stroke duration and duration of physiotherapy intervention of the participants were 54.2±12.5 years, 18.27±23.98 months and 13.04±15.09 months, respectively. Majority of the participants experienced musculoskeletal pain within the first 3 months after stroke. The most commonly affected body region was the shoulder (80.7%) followed by the wrists/hand (60.2%) and the least affected body region was the elbow (38.5%). The overall prevalence of musculoskeletal pain was 88%. The prevalence was significantly (χ2 =4.5, p-value=0.034) higher among males (57.8%) than females (42.2%). Conclusion: The study found high prevalence of musculoskeletal pain among stroke patients with males more commonly affected than females, and the shoulder being the most commonly affected joint. Assessing musculoskeletal pain and effective interventions for improving pain should constitute an integral part of a stroke rehabilitation plan

Knowledge and attitude of health professional students toward patients living with AIDS.

INTRODUCTION: What health professional students know of AIDS and their attitudes towards PLWA enrich our knowledge in assuring quality of care administered to AIDS patients. OBJECTIVES: This study was designed to assess 1) What Nigerian students in various health disciplines know about AIDS and how they behave towards PLWA. and 2) Determine the sociodemographic variables that could influence knowledge of AIDS and behaviour towards PLWA among students of the various health disciplines in a university in North- Eastern Nigeria. METHODS: This cross-sectional study involving student volunteers (n=644) in the last two years of their professional training drawn from six disciplines were surveyed using a two-part questionnaire. Section I of which elicited students' sociodemographic and previous AIDS encounter information, and section II assessed knowledge and behaviour towards PLWA. RESULTS: Students in surveyed health professions had an unsatisfactory level of knowledge on AIDS pathophysiology and their behaviour towards PLWA was negative. Gender, clinical year, religious affiliation, discipline, level of satisfaction with AIDS instructions, knowing a family member or another person with a diagnosis of AIDS and willingness to provide care for an AIDS patient influenced the students' knowledge and behaviour. CONCLUSION AND RECOMMENDATION: The study revealed a real possibility for health professional students to hesitate to care for PLWA, or render uncoordinated or fragmented care at the time of their graduation. It suggests the need for intervention to include methodical and all inclusive clinical clerkship on HIV/AIDS and small group discussions with real life case scenerios involving PLWA while in training.

In vivo relationship between monoamine oxidase type B and alcohol dehydrogenase: effects of ethanol and phenylethylamine.

The role of acute ethanol (2.5 g/kg i.p.) and phenylethylamine (100 mg/kg i.p.) on the brain and platelet monoamine oxidase activities, hepatic cytosolic alcohol dehydrogenase, redox state and motor behaviour were studied in male rats. Ethanol on its own decreased the redox couple ratio, as well as, alcohol dehydrogenase activity in the liver whilst at the same time it increased brain and platelet monoamine oxidase activity due to lower Km with no change in Vmax. The elevation in both brain and platelet MAO activity was associated with ethanol-induced hypomotility in the rats. Co-administration of phenylethylamine and ethanol to the animals, caused antagonism of the ethanol-induced effects described above. The effects of phenylethylamine alone, on the above mentioned biochemical and behavioural indices, are more complex. Phenylethylamine on its own, like ethanol, caused reduction of the cytosolic redox ratio and elevation of monoamine oxidase activity in the brain and platelets. However, in contrast to ethanol, this monoamine produced hypermotility and activation of the hepatic cytosolic alcohol dehydrogenase activity in the animals. The results suggest that some of the toxic actions of ethanol in rats may be mediated through the activation of monoamine oxidase type B, with the consequent depletion of the endogenous levels of phenylethylamine. The data appear to support the concept of phenylethylamine involvement in affective disorders.

Effects of beta-phenylethylamine on locomotor activity, body temperature and ethanol blood concentrations during acute ethanol intoxication.

Beta-phenylethylamine (PEA) is an endogenous amine which is metabolised by MAO B. The function of this enzyme is known to be modified by ethanol so we have studied the interactions of PEA with ethanol. Rectal temperatures of rats were determined and animals pretreated with ethanol (2.5 g kg-1 IP) 90 min before PEA 20, 40, 100 mg kg-1 IP). Spontaneous locomotor activity (SLA) was then recorded, for 30 min, temperatures redetermined and blood ethanol levels evaluated. PEA increased SLA but did not alter rectal temperatures, and at 40 mg kg-1 it not only attenuated ethanol hypothermia and blood levels but also modified ethanol hypomotility. The highest dose of PEA (100 mg kg-1) decreased blood ethanol concentration and sedation but did not counteract the hypothermia. Thus PEA increased ethanol clearance, though the underlying mechanism is not totally clear. This finding is discussed in relation to its catecholaminergic and enzyme inducing characteristics.

Effects of naloxone and other opiate antagonists on blood-ethanol concentration in acutely-ethanol-intoxicated rats.

The effects of naloxone hydrochloride (NAL) and other opiate antagonists on blood-ethanol concentration (BEC) in acutely-ethanol-intoxicated rats were examined. Using a 1 mg/kg body wt. dose of NAL, the maximum decrease in BEC was found to occur at 30 min. At 30 min after administration of various doses of NAL, it was found that BEC was decreased maximally by a 2 mg/kg dose, whereas the first significant decrease was caused by a 10 micrograms/kg dose. BEC was also decreased by naltrexone (1 mg/kg), but not by a 4 mg/kg dose of any of four Mr compounds (Mr 1452, Mr 1453, Mr 2266 and Mr 2267). It is suggested that pharmacokinetic antagonism of acute alcohol intoxication by naloxone and naltrexone is unrelated to the property of opiate antagonism, but may involve the ability of certain such antagonists to interact with hepatic NAD+-dependent oxidative metabolism.

Antagonism of acute alcohol intoxication by naloxone.

We have previously shown that proprietary naloxone hydrochloride (Narcan) reverses the disturbance of the redox states of the hepatic NAD(P) couples and causes a simultaneous lowering of blood-ethanol concentration in acutely-ethanol-intoxicated rats. We now confirm these findings by using pure naloxone hydrochloride and demonstrate the inability of the methyl-4-hydroxybenzoate preservative present in the Narcan ampoules to influence the above effects of ethanol.