Objectives:Although, Bell’s palsy (BP) is a well known and common condition in the community, its epidemiology is unclear. We aimed to estimate the epidemiology of BP in Al-Kharga district, New Valley Governorate, Egypt. Material and Methods:The present survey was conducted during the second stage of the project study (Epidemiology of Major Neurological Disorders in Al-Kharga district, New Valley Governorate) from 1 June 2006 to 31 May 2008. A total eligible population of 62 583 subjects was screened through a door-to-door survey by three specialists in neurology and 15 social workers. Detailed history of all subjects who had experienced facial paralysis at any point of time in their lives, was recorded through a specific questionnaire and meticulous neurological examination by neurologists. Results:One hundred patients were diagnosed to have BP, yielding a lifetime prevalence rate of 192.18/ 100 000 population aged 8 years and above. Lifetime prevalence rate was significantly higher among females than males (245.81 and 141.73/100 000, respectively), and among rural rather than urban inhabitants (281.14 and 156.63/100 000, respectively). The crude annual incidence rate of BP was significantly higher in the second year of the survey than in the first year (71.11/100 000 and 32.76/100 000, respectively). Male sex (P, 0.05),and facial pain from incomplete recovery (P#0.01) were predictors for poor BP outcomes. Conclusion:Bell’s palsy tends to occur in clusters, with higher incidence rates among females and rural inhabitants. The presence of concomitant facial pain, together with occurrence in male sex carries a poor prognosis.

Objectives:Although, Bell’s palsy (BP) is a well known and common condition in the community, its epidemiology is unclear. We aimed to estimate the epidemiology of BP in Al-Kharga district, New Valley Governorate, Egypt. Material and Methods:The present survey was conducted during the second stage of the project study (Epidemiology of Major Neurological Disorders in Al-Kharga district, New Valley Governorate) from 1 June 2006 to 31 May 2008. A total eligible population of 62 583 subjects was screened through a door-to-door survey by three specialists in neurology and 15 social workers. Detailed history of all subjects who had experienced facial paralysis at any point of time in their lives, was recorded through a specific questionnaire and meticulous neurological examination by neurologists. Results:One hundred patients were diagnosed to have BP, yielding a lifetime prevalence rate of 192.18/ 100 000 population aged 8 years and above. Lifetime prevalence rate was significantly higher among females than males (245.81 and 141.73/100 000, respectively), and among rural rather than urban inhabitants (281.14 and 156.63/100 000, respectively). The crude annual incidence rate of BP was significantly higher in the second year of the survey than in the first year (71.11/100 000 and 32.76/100 000, respectively). Male sex (P, 0.05),and facial pain from incomplete recovery (P#0.01) were predictors for poor BP outcomes. Conclusion:Bell’s palsy tends to occur in clusters, with higher incidence rates among females and rural inhabitants. The presence of concomitant facial pain, together with occurrence in male sex carries a poor prognosis.

Objectives:Although, Bell’s palsy (BP) is a well known and common condition in the community, its epidemiology is unclear. We aimed to estimate the epidemiology of BP in Al-Kharga district, New Valley Governorate, Egypt. Material and Methods:The present survey was conducted during the second stage of the project study (Epidemiology of Major Neurological Disorders in Al-Kharga district, New Valley Governorate) from 1 June 2006 to 31 May 2008. A total eligible population of 62 583 subjects was screened through a door-to-door survey by three specialists in neurology and 15 social workers. Detailed history of all subjects who had experienced facial paralysis at any point of time in their lives, was recorded through a specific questionnaire and meticulous neurological examination by neurologists. Results:One hundred patients were diagnosed to have BP, yielding a lifetime prevalence rate of 192.18/ 100 000 population aged 8 years and above. Lifetime prevalence rate was significantly higher among females than males (245.81 and 141.73/100 000, respectively), and among rural rather than urban inhabitants (281.14 and 156.63/100 000, respectively). The crude annual incidence rate of BP was significantly higher in the second year of the survey than in the first year (71.11/100 000 and 32.76/100 000, respectively). Male sex (P, 0.05),and facial pain from incomplete recovery (P#0.01) were predictors for poor BP outcomes. Conclusion:Bell’s palsy tends to occur in clusters, with higher incidence rates among females and rural inhabitants. The presence of concomitant facial pain, together with occurrence in male sex carries a poor prognosis.

Background Auditory functions among patients with type 2 diabetes mellitus (DM) are controversial regarding cochlear or neural changes and the relationship between these changes and serum level of glycosylated hemoglobin (HbA 1c %). Aim of the study The aim of the study was to investigate auditory dysfunctions in type 2 DM patients with poor versus good glycemic control. Materials and methods The present study was conducted on three groups: two diabetic groups with poor and good glycemic control (n = 18 and 14, respectively) based on serum HbA 1c % and one healthy control group (n = 30) matched with age, sex, and BMI. All participants were subjected to clinical assessment, audiometry, brainstem auditory evoked potential ( BAEP), and evoked acoustic emissions transient evoked otoacoustic emissions and distortion product otoacoustic emissions (TEOAEs and DPOAEs). Results Diabetic patients with poor glycemic control had significantly elevated hearing thresholds compared with other groups at low and high frequencies in audiometry (P 0.01 and P 0.001). They showed significantly prolonged absolute latency in wave I and interpeak latency ( III–V) in the BAEP test compared with other groups (P 0.001). DM patients with poor glycemic control had significantly low amplitudes at all frequencies in the TEOAE test, as well as at high frequencies (4 and 6 kHz) on the DPOAE test, compared with other groups (P 0.001 and P 0.05, respectively). There were significant correlations between HbA 1c % and interpeak latency III–V (r = 0.340, P = 0.004) on the one hand and overall response of TEOAE amplitude (r = −0.471; P = 0.000) on the other. Conclusion Diabetic patients with poor glycemic control had worse auditory dysfunctions on both cochlear and neural findings.

Considerable effort in recent years has been devoted to investigating neurophysiological changes in the brain after stroke and in developing novel strategies to enhance recovery particularly in the limbs and trunk. In contrast, although dysphagia is a severe complication and can be life threatening in a considerable number of stroke patients, it has not yet received the attention devoted to limb control. In this review, we discuss how introduction of (a) transcranial magnetic stimulation (TMS) to test noninvasively the integrity of the cortico-bulbar swallowing system and (b) the plasticity provoking protocols of rTMS and transcranial direct current stimulation have recently stimulated research into dysphagia after stroke and led to new potential avenues for treatment. We discuss the neural control of swallowing and discuss the contributions of TMS to understand how different brain areas are involved in dysphagia. We also consider recent studies using noninvasive brain stimulation to interact with synaptic plasticity in cortex and enhance recovery of dysphagia following stroke. Although further studies are needed, theseinvestigations provide an important starting point to understand the stimulation parameters and patient characteristics that may influence the optimal response to therapeutic noninvasive brain stimulation. These techniques need to be refined further through a multicenter study so that they can become an essential tool that can be used in academic centers of excellence as well as in a general hospital setting.

Considerable effort in recent years has been devoted to investigating neurophysiological changes in the brain after stroke and in developing novel strategies to enhance recovery particularly in the limbs and trunk. In contrast, although dysphagia is a severe complication and can be life threatening in a considerable number of stroke patients, it has not yet received the attention devoted to limb control. In this review, we discuss how introduction of (a) transcranial magnetic stimulation (TMS) to test noninvasively the integrity of the cortico-bulbar swallowing system and (b) the plasticity provoking protocols of rTMS and transcranial direct current stimulation have recently stimulated research into dysphagia after stroke and led to new potential avenues for treatment. We discuss the neural control of swallowing and discuss the contributions of TMS to understand how different brain areas are involved in dysphagia. We also consider recent studies using noninvasive brain stimulation to interact with synaptic plasticity in cortex and enhance recovery of dysphagia following stroke. Although further studies are needed, theseinvestigations provide an important starting point to understand the stimulation parameters and patient characteristics that may influence the optimal response to therapeutic noninvasive brain stimulation. These techniques need to be refined further through a multicenter study so that they can become an essential tool that can be used in academic centers of excellence as well as in a general hospital setting.

The potential protective effect of citicoline on aluminum chloride-induced cognitive deficits was investigated in rats. In a Morris water maze, administration of aluminum chloride to rats for 90 days resulted in increased escape latency to reach the platform and decreased swimming speed in acquisition trials. Similarly, in probe trials, the time required to reach the hidden platform was increased and the time spent in the target quadrant was reduced. Also, administration of aluminum chloride to rats for 90 days increased the reference and working memory errors and time required to end the task in the radial arm maze. In addition, this treatment decreased the step-through latency in the passive avoidance test. Concurrently, treatment of rats with aluminum chloride for 90 days increased hippocampal glutamate, malondialdehyde, and nitrite levels and decreased intracellular reduced glutathione level. In the citicoline-treated group, aluminum chloride-induced learning and memory impairments as assessed by the Morris water maze, radial arm maze, and passive avoidance tests were inhibited. At the same time, treatment of rats with citicoline prevented the biochemical alterations induced by aluminum chloride in the hippocampus. It can be concluded that elevation of hippocampal glutamate level with consequent oxidative stress and nitric oxide (NO) overproduction may play an important role in aluminum-induced cognitive impairments. Also, our results suggest, for the first time, that citicoline can protect against the development of these cognitive deficits through inhibition of aluminum-induced elevation of glutamate level, oxidative stress, and NO overproduction in the hippocampus.

The potential protective effect of citicoline on aluminum chloride-induced cognitive deficits was investigated in rats. In a Morris water maze, administration of aluminum chloride to rats for 90 days resulted in increased escape latency to reach the platform and decreased swimming speed in acquisition trials. Similarly, in probe trials, the time required to reach the hidden platform was increased and the time spent in the target quadrant was reduced. Also, administration of aluminum chloride to rats for 90 days increased the reference and working memory errors and time required to end the task in the radial arm maze. In addition, this treatment decreased the step-through latency in the passive avoidance test. Concurrently, treatment of rats with aluminum chloride for 90 days increased hippocampal glutamate, malondialdehyde, and nitrite levels and decreased intracellular reduced glutathione level. In the citicoline-treated group, aluminum chloride-induced learning and memory impairments as assessed by the Morris water maze, radial arm maze, and passive avoidance tests were inhibited. At the same time, treatment of rats with citicoline prevented the biochemical alterations induced by aluminum chloride in the hippocampus. It can be concluded that elevation of hippocampal glutamate level with consequent oxidative stress and nitric oxide (NO) overproduction may play an important role in aluminum-induced cognitive impairments. Also, our results suggest, for the first time, that citicoline can protect against the development of these cognitive deficits through inhibition of aluminum-induced elevation of glutamate level, oxidative stress, and NO overproduction in the hippocampus.

The potential protective effect of citicoline on aluminum chloride-induced cognitive deficits was investigated in rats. In a Morris water maze, administration of aluminum chloride to rats for 90 days resulted in increased escape latency to reach the platform and decreased swimming speed in acquisition trials. Similarly, in probe trials, the time required to reach the hidden platform was increased and the time spent in the target quadrant was reduced. Also, administration of aluminum chloride to rats for 90 days increased the reference and working memory errors and time required to end the task in the radial arm maze. In addition, this treatment decreased the step-through latency in the passive avoidance test. Concurrently, treatment of rats with aluminum chloride for 90 days increased hippocampal glutamate, malondialdehyde, and nitrite levels and decreased intracellular reduced glutathione level. In the citicoline-treated group, aluminum chloride-induced learning and memory impairments as assessed by the Morris water maze, radial arm maze, and passive avoidance tests were inhibited. At the same time, treatment of rats with citicoline prevented the biochemical alterations induced by aluminum chloride in the hippocampus. It can be concluded that elevation of hippocampal glutamate level with consequent oxidative stress and nitric oxide (NO) overproduction may play an important role in aluminum-induced cognitive impairments. Also, our results suggest, for the first time, that citicoline can protect against the development of these cognitive deficits through inhibition of aluminum-induced elevation of glutamate level, oxidative stress, and NO overproduction in the hippocampus.

The potential protective effect of citicoline on aluminum chloride-induced cognitive deficits was investigated in rats. In a Morris water maze, administration of aluminum chloride to rats for 90 days resulted in increased escape latency to reach the platform and decreased swimming speed in acquisition trials. Similarly, in probe trials, the time required to reach the hidden platform was increased and the time spent in the target quadrant was reduced. Also, administration of aluminum chloride to rats for 90 days increased the reference and working memory errors and time required to end the task in the radial arm maze. In addition, this treatment decreased the step-through latency in the passive avoidance test. Concurrently, treatment of rats with aluminum chloride for 90 days increased hippocampal glutamate, malondialdehyde, and nitrite levels and decreased intracellular reduced glutathione level. In the citicoline-treated group, aluminum chloride-induced learning and memory impairments as assessed by the Morris water maze, radial arm maze, and passive avoidance tests were inhibited. At the same time, treatment of rats with citicoline prevented the biochemical alterations induced by aluminum chloride in the hippocampus. It can be concluded that elevation of hippocampal glutamate level with consequent oxidative stress and nitric oxide (NO) overproduction may play an important role in aluminum-induced cognitive impairments. Also, our results suggest, for the first time, that citicoline can protect against the development of these cognitive deficits through inhibition of aluminum-induced elevation of glutamate level, oxidative stress, and NO overproduction in the hippocampus.