Lower lid entropion secondary to treatment with alpha-1a receptor antagonist: a case report

<p>Abstract</p> <p>Introduction</p> <p>The use of alpha-1a receptor antagonists (tamsulosin) is widely accepted in the treatment of benign prostatic hypertrophy (BPH). It has previously been implicated as a causative agent in intra-operative floppy iris syndrome due to its effects on the smooth muscle. We report a case of lower lid entropion that may be related to a patient commencing treatment of tamsulosin.</p> <p>Case presentation</p> <p>A 74-year-old Caucasian man was started on alpha 1-a receptor antagonist (Tamsulosin) treatment for benign prostatic hypertrophy. Eight days later, he presented to the ophthalmology unit with a right lower lid entropion which was successfully treated surgically with a Weiss procedure.</p> <p>Conclusion</p> <p>We report a case of lower lid entropion that may be secondary to the recent use of an alpha-1a blocker (tamsulosin). This can be explained by considering the effect of autonomic blockade on alpha-1 receptors in the Muller's muscle on a patient that may already have an anatomical predisposition to entropion formation due to a further reduction in muscle tone.</p

Effect of brimonidine tartrate 0.15% on scotopic pupil size and upper eyelid position: controlled trial

BACKGROUND: To evaluate the effect of brimonidine tartrate 0.15% ophthalmic solution on pupil size under scotopic condition and upper eyelid position. METHODS: This study comprised 72 eyes of 36 healthy subjects. A single drop of brimonidine tartrate 0.15% ophthalmic solution was instilled in the right eye and artificial tear was instilled in the left eye. Pupil size was measured using an infra-red pupillometer under scotopic condition before and at 30 min, 2, 4, 6, 8 and 10 h after instillation. Measurement of margin reflex distance 1 (MRD1) was performed using a millimetre ruler before and after at 10 min after instillation. RESULTS: The mean age of the subjects was 32.19 ± 11.43 years (range 10–52 years), 17 were female and 19 were male. Before brimonidine instillation, the mean pupil size was 6.09 ± 1.03 mm in the brimonidine eyes and 6.06 ± 1.04 mm in the control eyes. There was a significant decrease in mean pupil size at 30 min (4.45 ± 1.04), 2 h (4.49 ± 1.06), 4 h (4.59 ± 1.06), 6 h (4.89 ± 1.06) and 8 h (5.38 ± 1.02) after instillation compared to before in brimonidine eyes (p < 0.001 for all). There was a significant miosis continued for at least 6 h (5.95 ± 1.03) in control eyes (p < 0.001). There was no significant change in MRD1, before and after instillation both in brimonidine and control eyes. CONCLUSIONS: Brimonidine tartrate 0.15% had a significant miosis under scotopic condition for at least 8 h after instillation and had a significant miosis on the untreated eye for at least 6 h

PET and SPECT Imaging in Dystonia

Dystonia is a syndrome characterized by involuntary, sustained muscle contractions causing twisting movements and abnormal postures. It is a common movement disorder with different forms that can be classified based on different clinical characteristics. Idiopathic focal dystonia (dystonia in one body part with no known cause) is the most common form. The more generalized (throughout the body) forms of dystonia have a younger age of onset and usually an underlying genetic defect. The mode of inheritance is usually autosomal dominant. Of these, the most common are DYT-TOR1A and DYT-THAP1 dystonia. In combined dystonia syndromes, also autosomal dominantly inherited disorders, dystonia patients have additional neurological symptoms (e.g., parkinsonism or myoclonus). This group includes dopamine-responsive dystonia, myoclonus-dystonia, rapid-onset dystonia-parkinsonism, and paroxysmal dystonia. In this chapter, we describe results from positron emission tomography (PET) and single-photon emission computed tomography (SPECT) studies in the different forms of dystonia. Three different kinds of PET and SPECT techniques have been used in patients with dystonia: glucose metabolism scans, regional cerebral blood flow studies, and receptor imaging. Increased glucose metabolism was found in the basal ganglia, thalamus, and cerebellum of patients with different forms of focal dystonia and in DYT1 dystonia. Patients with DYT6 dystonia showed decreased glucose metabolism in the putamen. Results from regional cerebral blood flow (rCBF)-activation studies differed extensively among different studies and different patient groups, mainly because of study design. Overall, the primary and secondary motor and sensory cortices were found to be abnormal in almost all forms of dystonia, although the direction of the abnormalities differed. Dopamine was found to play a role in dystonia reflected by decreased dopamine D2/3 receptor binding in the striatum of patients with almost all forms of dystonia. In recent years, it has been established that other neurotransmitter systems, such as serotonin and gamma aminobutyric acid (GABA) also play a role in dystonia. In conclusion, dystonia is likely to be a network disorder with abnormalities in a large number of cortical and subcortical areas. There might be a central role for the basal ganglia with abnormalities in dopamine receptor binding, as well as other neurotransmitter systems