Tehran University Medical Journal

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Defining the patient outcome and decision making about allocation of our limited fund and technology for comatose patients depends on our knowledge about frequency and outcome of various coma etiologies. We determined the various coma causes frequency and one-month outcome of non traumatic coma. . In addition the co existence of the primary neurologic signs with the one-month outcome of non traumatic coma was defined.
Methods and Materials: Our study is based on 130 comatose patients in a one-year study in Sina Hospital that consisted of 80 non traumatic and 50 traumatic patients.
Results: 74% of the cases were men and 26% were women. The most common etiology of coma was trauma (38.5%). The other common etiologies were cerebro‌vascular diseases (25.4%), cancer (10%) and hypoxia-ischemia (8.5%). The most common cause of coma in men was trauma (46.9%) while the vascular diseases were the most common etiology of coma in women (41.2%).In under 40 year patients trauma was the cause of coma in 57.5% of cases in respect to 28% in above 40 cases. On the other hand, vascular diseases and malignancies were the etiology of coma in 15% of under 40 year patients and 46.5% of above 40 year patients. Among traumatic etiologies of coma, subdural hematoma was the most frequent (40%). In our research none of patients who did not have one of pupillary, oculocephalic or motor reflexes in the 3rd and 7th day of the onset of coma had acceptable outcome after one month. With consideration of pupillary, corneal, oculocephalic and motor reflexes in combination, loss of at least two of them in the 3rd and 7th day accompanied with no acceptable outcome. On the other hand the presence of three or more reflexes in the 3rd and 7th day of coma was a good prognostic factor, with 80% and 88.9% chance of acceptable recovery respectively.
Conclusion: According of the study, the best time for prediction of outcome in a comatose patient, is the third or seventh the day after the onset of coma. Also relay on combination of brain stem reflexes, gives us more acceptable result.

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 Background: Approximately 5-10% of epileptic patients do not respond to antiepileptic drugs. Adenosine has an inhibitory effect on the nervous system and its metabolism is prevented as a side effect of allopurinol, a xanthine oxidase inhibitor. The current study evaluates the efficacy of allopurinol in intractable epilepsy.

Methods: In this double-blind case-control clinical trial, of the 38 epileptics with intractable seizures, 18 received 300 mg allopurinol daily and 20 received a placebo as adjuvant treatment to their previous antiepileptic drugs. The patients were first examined two weeks after initiation of the treatment and then monthly for a total of six months, during which they were evaluated for seizure control and possible side effects.

Result: Of the 38 participants, 32 patients completed the study. There were significant differences between the two groups in terms of reduction in the total number of seizures over the entire six-month trial. A seizure reduction of 30% observed in 66% of the patients, 50% in 55%, and 60% in 44% of the cases in the allopurinol group was achieved after two months and persisted throughout the study. Furthermore, a significant difference in seizure duration was found between the two groups in month four of the trial. In the allopurinol group, two patients had transient rashes, two patients had mild nausea, and two experienced dizziness however, only one patient discontinued the drug due to dizziness. In the placebo group, one patient had rash and one had nausea. In addition, no significant hematological or hepatic changes were found during the trial in either group.

Conclusions: The results suggest that allopurinol is a safe and effective adjuvant agent in refractory epilepsy. Based on this study, we suggest that purine metabolic pathways and the specific use of allopurinol should be further investigated for the treatment of refractory epilepsy.