Pregabalin as a Neuroprotector after Spinal Cord Injury in Rats: Biochemical Analysis and Effect on Glial Cells

As one of trials on neuroprotection after spinal cord injury, we used pregabalin. After spinal cord injury (SCI) in rats using contusion model, we observed the effect of pregabalin compared to that of the control and the methylprednisolone treated rats. We observed locomotor improvement of paralyzed hindlimb and body weight changes for clinical evaluation and caspase-3, bcl-2, and p38 MAPK expressions using western blotting. On histopathological analysis, we also evaluated reactive proliferation of glial cells. We were able to observe pregabalin's effectiveness as a neuroprotector after SCI in terms of the clinical indicators and the laboratory findings. The caspase-3 and phosphorylated p38 MAPK expressions of the pregabalin group were lower than those of the control group (statistically significant with caspase-3). Bcl-2 showed no significant difference between the control group and the treated groups. On the histopathological analysis, pregabalin treatment demonstrated less proliferation of the microglia and astrocytes. With this animal study, we were able to demonstrate reproducible results of pregabalin's neuroprotection effect. Diminished production of caspase-3 and phosphorylated p38 MAPK and as well as decreased proliferation of astrocytes were seen with the administration of pregabalin. This influence on spinal cord injury might be a possible approach for achieving neuroprotection following central nervous system trauma including spinal cord injury.

Is Electrical Stimulation Beneficial for Improving the Paralytic Effect of Botulinum Toxin Type A in Children with Spastic Diplegic Cerebral Palsy?

PURPOSE: The purpose of the present study was to investigate whether electrical stimulation (ES) improves the paralytic effect of botulinum toxin type A (BTX-A) and evaluate the differences between low frequency (LF) and high frequency (HF) ES in children with spastic diplegic cerebral palsy (CP). MATERIALS and METHODS: Twenty-three children with spastic diplegia CP who had BTX-A injections into both gastrocnemius muscles were assessed. Following the toxin injection, electrical stimulation was given to 1 side of the injected muscles and a sham-stimulation to the other side for 30 min a day for 7 consecutive days [HFES (25Hz) to 11 children, LFES (4Hz) to 12 children]. The compound motor action potentials (CMAP) from the gastrocnemius muscle were assessed before injection and at 5 time points (days 3, 7, 14, 21, and 30) after injection. The clinical assessments of spasticity were performed before and 30 days after injection. RESULTS: The CMAP area became significantly lower in both LFES and HFES sides from 3 days after injection compared to baseline values. In other words, the CMAP area of the sham-stimulated side showed a significant decrease at 7 or 14 days after injection. However, there were no significant differences in clinical assessment of spasticity between the stimulated and sham-stimulated sides. CONCLUSION: Short-term ES in both LF and HF to the spastic muscles injected with BTX-A might induce earlier denervating action of BTX-A. However, it does not necessarily lead to clinical and electrophysiological benefits in terms of reduction of spasticity.

Short course of oral prednisolone on disappearance of lesion and seizure recurrence in patients of solitary cysticercal granuloma with single small enhancing CT lesion: an open label randomized prospective study.

OBJECTIVE: To evaluate the effect of a short course of oral prednisolone on disappearance of lesion and seizure recurrence in newly diagnosed patients with single small enhancing CT lesion. METHODS: In this open-label, randomized, prospective follow-up study, 100 patients of new-onset seizures and a cysticercus granuloma presenting as single enhancing computed tomography detected lesion were randomly divided in two groups to receive either antiepileptic monotherapy (Group A) or antiepileptic drugs with oral prednisolone in a dose of 1 mg/kg body weight for 7 days and tapering off dose in next 3 days (Group B). Repeat CT scan was performed on 8th-12th week to know radiological state of lesion. The patients were followed up for 1 year for seizure recurrence. RESULTS: The majority of patients were in second decade. Male: female ratio 1.56:1. Mean number of seizure episodes was 4.33 +/- 3.50 in group A and 4.23 +/- 3.97 in group B. Partial seizure were the most common presentation (85%). 72% patients presented with single seizure or seizure in cluster. Solitary ring lesion was the commonest (69%) CT finding, most of them were located in parietal lobe (52%). Follow up CT scan showed complete resolution of lesion in 60.86% of total [group A (n = 47), 32 patients, 68.08%; group B (n = 45), 24 patients, 53.33%]. Significant difference in group A and B regarding lesion resolution was observed (chi2 = 5.926, d.f. = 1) p < 0.05. Clinical follow up showed seizure recurrence in group A - 5 patients (10.63%), in group B - 12 patients (26.66%). Statistically significant higher number of seizure recurrences were noted in group B as compared to group A (chi2 = 3.93, d.f. = 1) p < 0.05. CONCLUSIONS: Short-term oral prednisolone along with antiepileptic drugs helps in rapid resolution of single small enhancing lesions in patient with newly diagnosed seizure disorder with good clinical outcome.

Do we need anti snake venom (ASV) for management of elapid ophitoxaemia.

Twelve patients of elapid ophitoxaemia presented with neuromuscular paralytic features were given anticholinesterase (Neostigmine) in recommended dosage. In four of these patients, despite neuromuscular paralysis, no ASV was used. All these four patients survived. In eight patients, ASV was used; in three of whom it used in doses less than 50 units, yet patients survived. Of the remaining five, despite use of ASV in higher doses (more than 50 units), two succumbed to death. Eight patients required ventilatory support. Hence, in absence of any definite role of ASV in management of elapid ophitoxaemia (snake bite), use of anticholinesterase drugs alone, with good supportive care and prevention of likely complications, can result in satisfactory outcome.

Hypokalaemic periodic paralysis in central Sri Lanka.

We describe 14 Sinhalese male patients with hypokalaemic periodic paralysis (HPP). The age at onset was between 10 and 32 years. Each paralytic episode lasted from 6 to 48 hours (except in one patient who had an attack lasting 5 days). The frequency of attacks varied from 8 to 10 per month in one patient to only 2 attacks over a period of 16 years in another. Four patients (28.6%) had a family history of the disease. Hypokalaemia (serum potassium 1.5 to 3 mmol/l) was documented during an attack in 11 patients. No cause for hypokalaemia was evident in any of them. Investigations including EMG, thyroid hormone level and skeletal muscle histology were within normal limits between episodes. All the patients responded well to treatment with potassium supplementation, alone or with acetazolamide.

Hyperkalemic periodic paralysis associated with thyrotoxicosis.

A 32 year old male presented with episodic pure motor weakness for 1 1/2 months. On evaluation he was found to be thyrotoxic. Hyperkalemic challenge test provoked similar weakness with raised serum potassium (6 meq/L). He responded to treatment with neomercazole. Till he became euthyroid, he responded to the addition of acetazolamide to his medication. He is symptom free on antithyroid drug alone over 8 months of follow up.

Hypokalemic paralysis.

A case of Hypokalemic paralysis is reported which had an atypical onset and clinical features. The paralysis totally recovered on replacement of potassium.

Parálisis periódica tirotóxica / Tyrotoxic periodic paralisys

La parálisis tirotóxica ocurre mucho más frecuentementeen orientales que en blancos y ha sido informada muy rara vez en pacientes descendencia hispana. Un hombre hondureño de 36 años de edad se presentó con debilidad de los miembros inferiores después de hacer ejercicio excesivo. Los hallazgoslaboratoriales revelan hipokalemia severa (2.3 mEq/L) e hipertiroidismo. La administración del cloruro de Potacio resultó en la normalización de la debilidad muscular. El tratamiento con propanolol y la subsecuente restauración del estado eutiroideos como metimazol 10 mg p.o. c/8 horas, fue efectivo para prevenir futuros episodios de parálisis. La parálisis periódica tirotóxica, aunque rara en pacientes hispanos, debe ser considerada en el diagnóstico diferencial de debilidad muscular en ésta población

Hypokalemic periodic paralysis: a rarely considered diagnosis in the pediatric patient

Un paciente varón de 14 años de edad es hopitalizado con episodios repetidos de debilidad generalizada e hipocalemia (1.3 meq/L). La parálisis desaparece al corregir el potasio con líquidos endovenosos. El paciente permaneció asintomático, excepto por una recaída, mediante dieta y suplementación oral de potasio. La parálisis periódica hipocalémica es una condición rara cuya primera manifestación ocurre en la adolescencia. Es causada por desequilibrios en los niveles de potasio sérico. Las dietas bajas en carbohidratos, suplementos de potasio, espironolactona y acetazolamida se han usado como agentes para estabilizar el potasio sérico y disminuir la frecuencia de los ataques paralíticos