Sixth nerve palsy + ipsilateral Horner's syndrome = Parkinson's syndrome

To present five patients with VIth nerve palsy and ipsilateral Horner's Syndrome [HS], as a result of cavernous sinus alteration. Consecutive case series. Five patients presented abducens palsy with horizontal diplopia [3 in primary position and 2 in lateral gaze only] and ipsilateral HS. Apraclonidine 0.5% drops evidenced sympathetic denervation in all patients 40-60 min after instillation. All 5 cases had neuroimages [MRI in 3 cases, Computerized Tomography - CT in one case and Magnetic Resonance Angiography - MRA in one case] demonstrating cavernous sinus lesions; 2 meningiomas, 1 carotid-cavernous aneurism, 1 foreign body [bullet] and 1 squamous cell carcinoma. Lesions on the cavernous sinus need to be considered in cases of abducens nerve palsy and ipsilateral Horner's Syndrome

Irreversible Horner's syndrome diagnosed by aproclonidine test due to benign thyroid nodule

We are reporting an irreversible Horner Syndrome [HS] in a patient with benign thyroid gland nodule in which thyroidectomy was performed for treatment. A 37-year-old female was admitted to our clinic with a swelling in the left lobe of the thyroid gland and ptosis at the left eyelid. The clinical diagnosis of HS was confirmed pharmacologically by aproclonidine. Histopathologic examination of thyroidectomy specimen was reported as benign nodule. To the best of our knowledge, this is a very rare report in terms of thyroid benign nodule associated with irreversible HS due to cervical sympathetic chain compression

Spectrophotometric and potentiometric methods for the determination of cefprozil, dropropizine and tizanidine hydrochloride in pharmaceutical preparations

Two simple, accurate spectrophotometric and potentiometric methods were developed for the determination of cefprozil, dropropizine and tizanidine hydrochloride in their pharmaceutical preparations. The spectrophotometric method is based on the selective oxidation of cefprozil or tizanidine with N-bromosuccinimide in an alkaline medium to given an intense yellow product with a maximum absorption at 396 or 384 nm, respectively. The reaction conditions were studied and optimized. The reaction obeyed Beer's law over the concentration range 5-40 and 10-80 micro g mI[-1] for cefprozil and tizanidine hydrochloride, respectively. The potentiometric method involves the direct titration of cefprozil and dropropizine with N-bromosuccinimide in sulphuric acid medium and the end point is determined potentiometrically using platinum electrode. Cefprozil and dropropizine can be determined quantitatively in the concentration range of 0.13-1.30 and 0.118-1.180 mg with recovery values of 98.46-100.77 and 99.58-100.85% and relative standard deviations 0.39-0.54 and 0.52-0.87% for cefprozil and dropropizine, respectively. The proposed methods are applied for the determination of these drugs in pure forms and in pharmaceutical preparations

Inhibitory Effect of Fentanyl on Phenylephrine-Induced Contraction of the Rat Aorta

PURPOSE: Fentanyl was reported to inhibit the alpha1-adrenoceptor agonist-induced contraction. The goal of this in vitro study was to identify the alpha1-adrenoceptor subtype primarily involved in the fentanyl-induced attenuation of phenylephrine-induced contraction in isolated endothelium-denuded rat aorta. MATERIALS AND METHODS: Aortic rings were suspended in order to record isometric tension. Concentration-response curves for phenylephrine (10-9 to 10-5 M) were generated in the presence or absence of one of the following drugs: fentanyl (3x10-7, 10-6, 3x10-6 M), 5-methylurapidil (3x10-8, 10-7, 3x10-7 M), chloroethylclonidine (10-5 M) and BMY 7378 (3x10-9, 10-8, 3x10-8 M). Phenylephrine concentration-response curves were generated in the presence or absence of fentanyl in rings pretreated with either 3x10-9 M prazosin, 10-9 M 5-methylurapidil or 3x10-9 M BMY 7378. RESULTS: Fentanyl (10-6, 3x10-6 M) attenuated phenylephrine-induced contraction in the rat aorta. 5-Methylurapidil and BMY 7378 produced a parallel rightward shift in the phenylephrine concentration-response curve. The pA2 values for 5-methylurapidil and BMY 7378 were estimated to be 7.71 +/- 0.15 and 8.99 +/- 0.24, respectively. Fentanyl (10-6 M) attenuated phenylephrine-induced contraction in rings pretreated with 10-9 M 5-methylurapidil, but did not alter the rings when pretreated with 3x10-9 M BMY 7378. Pretreatment of the rings with chloroethylclonidine showed a 72.9 +/- 2.3% reduction in phenylephrine-induced maximal contraction. CONCLUSION: The results suggest that fentanyl attenuates phenylephrine-induced contraction by inhibiting the pathway involved in the alpha1D-adrenoceptor-mediated contraction of the rat aorta.

Efficacy of thiocolchicoside in Indian patients suffering from low back pain associated with muscle spasm.

Low back pain (LBP), a high prevalent condition among middle aged population, is usually associated with 'muscle spasm' that is responsible for giving rise to pain as well as its persistence. Muscle spasm is an involuntary, painful contraction of muscles that interferes with the function and cause of muscular disorder. Therefore centrally acting skeletal muscle relaxants, also called lissive drugs, are commonly used for its treatment. Sometimes these are combined with NSAIDs. The use of centrally acting skeletal muscle relaxants, though efficacious, is associated with frequent development of dose-related adverse drug reactions like sedation, impairment of voluntary motor functions and ataxia. So there is an urgent need for newer better drugs for treatment of conditions associated with muscle spasm. The objective of this study was to assess the efficacy and safety of oral thiocolchicoside (TC), a natural glycoside as compared to an adrenergic alpha 2 agonist tizanidine (TZ) in the Indian patients with LBP accompanied by muscle spasm. In this randomised, non-cross over clinical study, 60 adult Indians aged between 18 and 65 years with clinical diagnosis of muscle spasm associated with low back pain were enrolled. Patients satisfying the inclusion and exclusion criteria were either treated with TC and TZ for one week duration. Visual analogue scale (VAS) for pain at rest and VAS for tiredness, drowsiness, dizziness and alertness was used as the self-rated primary efficacy and safety variable. Pain was also assessed by mobility assessment; muscle spasm assessment and analgesic consumption. Data obtained from 58 patients (those who completed the study) indicated that in this one week study both TC and TZ provided sustained symptoms relief compared with the baseline. There was statistically significant reduction in severity of symptoms from day 0 to day 7 in both the groups. Patients were followed up on 3rd and 7th day and severity score of various parameters was recorded. There was significant difference among the treatment groups in favour of TC than TZ in efficacy parameters thus showing TC is at slightly better effective than TZ and in case of safety, TC scores significantly better over TZ in the patients with accompanying muscle spasm. These findings confirm that TC is a preferred option for the LBP with muscle spasms.

Involuntary jerking of lower half of the body (spinal myoclonus).

A 55 years old, hypertensive, diabetic lady presented with sudden onset jerky movement of lower trunk and legs. It was present both in awake and sleep and got aggravated by mental stress as well as sensory stimulation. Examination revealed rhythmic jerks affecting muscles of lower abdomen and legs. The lower limbs had normal muscle bulk and power, increased tone, exaggerated deep tendon reflexes, bilateral flexor plantar response with normal sensory autonomic and cerebellar function. Investigations including CSF study, MRI of dorsal spine and NCV were normal. A combination therapy with tizanidine, baclofen and clonazepam induced gradual improvement within 6 weeks.

Apraclonidine a 1 por cento em olhos submetidos à trabeculoplastia por laser de argônio / 1 percent apraclonidine in the eyes submitted in argon laser trabeculoplasty

Um estudo prospectivo, duplo-mascarado, com apraclonidine a 1 por cento e placebo em 30 olhos fácicos de 15 pacientes submetidos a trabeculoplastia por laser de argônio, foi realizado com a finalidade de determinar se havia diferença na variaçäo da pressäo intra-ocular no pré e pós-operatório e se havia correlaçöes entre a variaçäo da pressäo intra-ocular e a amplitude do ângulo da câmara anterior. Dos 15 pacientes, 10 do sexo feminino e 5 do sexo masculino, a idade variou de 33 a 78 anos (média de 60,9 anos). Todos os olhos eram portadores de glaucoma primário de ângulo aberto. O estudo foi dividido em duas fases, denominadas pré-laser e laser e a emplitude do ângulo da câmara anterior classificada em ampla e muito ampla. A relaizaçäo da fase pré-laser foi um bom parâmetro para a análise do comportamento da pressäo intra-ocular e também um bom indicador do tempo onde ocorrerá maior diminuiçäo da pressäo intra-ocular, após trabeculoplastia por laser de argônio. A amplitude, do ângulo da câmara anterior influenciou no comportamento da pressäo intra-ocular imediatamente após trabeculoplastia por laser de argônio. Conclui-se que a apraclonidine tem sua principal indicaçäo nos pacientes de ângulo de câmara anterior muito amplo após trabeculoplastia por laser de argônio, com a finalidade de diminuir a pressäo intra-ocular.

Effect of apraclonidine hydrochloride on acute introacular pressure rise after argon laser iridotomy

To determine the effect of apraclonidine hydrochloride on the acute intraocular pressure (IOP) rise after argon laser iridotomy (ALI), a double-masked comparative study was carried out. Twenty-nine eyes (20 patients) with angle-closure glaucoma underwent ALI. Eighteen eyes were treated with apraclonidine, and the remainder received a placebo 1 hour before and immediately after ALI. The mean IOP increase in the apraclonidine group was lower than that in the placebo group at each postlaser interval (p or = 10 mmHg. However, that kind of IOP rise was not found in the apraclonidine group (0 out of 18 eyes) (p < 0.01). Ocular or systemic side effects were not found in a series of examinations in both groups. Therefore, apraclonidine proved to be effective in lowering the IOP rise after ALI.

Tratamiento de la contractura muscular postraumática o por ejecicio con un nuevo agente mioespasmolítico: tizanidina (DS 103-282) / Treatment of post-traumatic or exercise induced muscle spasm with a new myopasmothic agent: tizanidine (DS 103-282)

En un estudio abierto, prospectivo a corto plazo se incluyeron 25 pacientes de uno u otro sexo, con edades comprendidas entre 16 a 60 años y con rigidez por cocntractura muscular consecutiva a traumatismo o ejercicio. A cada paceinte se le administró un nuevo mioespasmolítico: tizanidina por vía oral a dosis de 4 mg cada 8 horas durante 5 días. Se valoró en todos los casos, al inicio del estudio y a los 3 y 5 días de tratamiento el dolor espontáneo, el dolor a la palpación, la tensión muscular y la incapacidad funcional. También se valoraron los efectos seccundarios que se presentaron durante la administración de la tizanidina. Se notó una importante mejoría en los cuatro parámetros estudiados desde el tercer día de tratamiento, misma que se mantuvo hasta el final del estudio. El medicamento fue bien tolerado a dosis de 12 mg ya que el 68% de los pacientes no presentaron ningún efecto secundario. Se concluye que la tizanidina es una buena alternativa para el tratamiento de las contracturas musculares postraumáticas y por ejercicio

Characterization of lnhibition by Nifedipine and Nitroprusside of the Pressor Respones to alpha1-Adrenoceptor Agonists Cirazoline and Sgd 101/75 in Pithed Rats

In this study the effects of two unrelated vasodilators, nifedipine and nitroprusside, on the pressor responsiveness to the 1-adrenoceptor full agonist cirazoline and partial agonist Sgd 101/75 in pithed rats were examined. The experiments were performed on the vasoconstriction which was mediated by newly synthetized 1-adrenoceptors after removal of existing 1-adrenoceptors by phenoxybenzamine treatment(5mg/kg, i. p.). The t1/2 for recovery of the maximum response and ED50 of cirazoline were 23.1 +/- 5.5 and 26.9 +/- 7.4 hours, respectively, while that for recovery of the maximum response of Sgd 101/75 was 59.2 +/- 18.9 hours. The relationship between the pressor response and the fractional receptor occupancy for cirazoline showed a rectangular hyperbola. This occupancy-response curve markedly shifted to the right one day after phenoxybenzamine and subsequently returned to the control, indicative of a large receptor reserve. However, for Sgd 101/75 the occupancy-response curve exerted less of a hyperbola and shifited little after phenoxybenzamine. While the maximum response to cirazoline in the control rats was resistant to inhibition by the calcium entry blocker nifedipine, this resistance was significantly reduced one and 3 days after phenoxybenzamine, just as the maximum response to Sgd 101/75 was sensitive to nifedipine in the control rats. Likewise, when nitroprusside was used instead, the results were similar for the cirazoline and Sgd 101/75 effects. In summary, it seems unlikely that the resistance to the calcium entry blocker of the full agonist effect can be wholly ascribed either to the receptor reserves or to the differential calcium utilization itself. Alternatively, it is suggested that the differential resistance to calcium antagonists can result from the magnitude of the variables involved in the activation of 1-adrenoceptor coupling processes depending on the full or partial agonist.

Protective effect of ST-93 against ouabain induced arrhythmias in guinea pigs.

ST-93, a clonidine analog was studied for its antiarrhythmic activity in anaesthetised guinea pigs against ouabain induced arrhythmia. The amount of ouabain required (micrograms/kg) for the production of ventricular premature best. Ventricular fibrillation and cardiac arrest was recorded in control and drug treated group of animals. Both ST-93 and clonidine produced significant antiarrhythmic effect in guinea pigs. This protective effect was significantly blocked by yohimbine, suggesting that the antiarrhythmic effect is mediated through presynaptic alpha 2-adrenoceptors.