Ptosis could be caused by oculomotor nerve palsy in the midbrain infarction. Bilateral ptosis has been reported in several reports, which focused on clinical characteristics of midbrain infarction. Little research attention has been paid to the treatment of patients with bilateral ptosis in midbrain infarction. We experienced a case of severe bilateral ptosis occurring after midbrain infarction. The patient could not open her eyes, perform basic activities or achieve effective rehabilitation. Neurogenic ptosis can improved after the underlying cause is treated. However, in this case, bilateral ptosis was not improved after conservative care for 6 months and the patient remained limited in activities of daily living and mobility. Surgical correction of bilateral ptosis was done by the resection of both Muller's muscles. After surgical correction, the bilateral ptosis was much improved and the effect persisted for at least 6 months.
Citations
Cephalic tetanus is defined as a combination of trismus and paralysis of one or more cranial nerves. Cranial nerves III, IV, VI, VII, and XII may be affected, but the facial nerve is most frequently implicated. A 64-year-old female visited hospital for left ptosis followed by facial palsy after a left forehead abrasion in a car accident. At nine days post injury, left ptosis developed, left facial palsy developed twelve days post injury, and at fifteen days post injury, trismus and dysphagia developed. The following day, there was progression of symptoms to generalized tetanus, such as dyspnea and generalized rigidity. Videofluoroscopic swallow study showed penetration and aspiration. We report a case of cephalic tetanus with ptosis, facial palsy, and dysphagia, which progressed to generalized tetanus.
Citations
Method Twenty seven rats with a model of complete spinal cord injury were assigned to one of the following groups: control (n=9), electrical stimulation (n=10), and exercise (n=8) groups. After a 2-week intervention period, they were sacrificed, and the pattern of apoptosis was analyzed by in situ DNA nick-end labeling (TUNEL), by DNA fragmentation assay, and by Western blot for Bax and Bcl-2 using specimens from the right hamstring muscles for all groups.
Results The electrical stimulation group had increased apoptosis compared to the control group possibly due to overwork weakness, but there was no statistical significance between the groups. Apoptosis decreased in the exercise group compared with in the electrical stimulation and control group. The expression of Bcl-2 was most prominent in the exercise group, and it was significantly reduced in the electrical stimulation and control group.
Conclusion These findings suggest that exercise could play an important role in decreasing apoptosis by the up-regulation of Bcl-2 protein expression and that electrical stimulation might cause overwork weakness in rat models of spinal cord injury.
Method: We used 15 mdx and 15 control mice. To grade exercise loading, control and mdx mice were divided into free-living, exercise and immobilization groups. Free-living and exercise groups were further divided into steroid-treated and sham-treated groups to evaluate the effect of steroid administration. We measured the apoptotic changes using in situ DNA nick-end labling (TUNEL), DNA fragmentation assay and western blots for Bcl-2 and BAX.
Results: With TUNEL method, the largest number of myonuclei became positive in sham-treated exercise group while apoptosis was significantly reduced in steroid-treated exercise group in mdx mice. Steroid-treated free-living group showed higher rate of apoptotic change than sham-treated free-living group. With western blots for Bcl-2 and BAX, the value of BAX/Bcl-2 ratio was highest in sham-treated exercise group and among free living mdx mice, it was higher in steroid-treated group than sham-treated one.
Conclusion: Apoptosis can be minimized in free living condition while exercise loading or immobilization can cause apoptotic change in muscular dystrophy animal model. Steroid administration induces apoptosis in free living muscle and it alleviates apoptotic damage caused by exercise loading in mdx mice. (J Korean Acad Rehab Med 2003; 27: 232-239)
First
Prev
