topiramate and Hemorrhage

Topics: Anticonvulsants; Blood Platelets; Contusions; Epistaxis; Fructose; Hemorrhage; Humans; Neuroprotective Agents; Risk Assessment; Topiramate; Valproic Acid

Self-mutilation is direct and deliberate harm to one's body without conscious intent to die. It is observed in both men and women with various psychiatric disorders, but most of those who self-mutilate are women diagnosed with borderline personality disorder. Cocaine addiction is a significant worldwide public health problem, associated with somatic, psychological, psychiatric, socioeconomic and legal complications. Amphetamine use, but not cocaine use, has previously been associated with severe self-injurious behavior.. We report here a case of a female patient with recurring self-injurious behavior ("the pleasure of bleeding") induced by cocaine abuse.. The clinical characteristics of self-mutilation are manifold and there is a lack of agreement about its etiology. The complex behavior associated with cocaine abuse may be one cause of self-mutilation. Dysfunction of the inhibitory brain circuitry caused by drug addiction could explain why this cocaine-addicted patient loses control and self-mutilates during cocaine use.

Topics: Administration, Inhalation; Adult; Cocaine; Cocaine-Related Disorders; Female; Forearm; Fructose; Hemorrhage; Humans; Neuroprotective Agents; Self Mutilation; Topiramate; Treatment Outcome

Because topiramate (TPM) suppresses voltage-sensitive Na+ channels and non-N-methyl-D-aspartate (NMDA) receptors and enhances gamma-aminobutyric acid (GABA)-mediated inhibition, we tested whether it would protect against cerebral ischemia. The right middle cerebral artery (MCA) was embolized by an intra-arterial injection of autogenous thrombus. Two hours after thrombus injection, animals received intra-peritoneal injections (i.p.) of normal saline as control (n=6) or alternatively, a low- (20 mg/kg, i.p., n=6) or high-dose (40 mg/kg, i.p., n=6) of TPM. Neurological deficit was scored at 2 h and 24 h following the ischemic insult. The animals were sacrificed 24 h after ischemia and the coronal brain sections were stained with 2% 2,3,5-triphenyltetrazolium chloride (TTC) for determination of the percentage of infarct volume. Administration of TPM significantly improved the 24-h neurological deficit scores (low dose, 1.75+/-0.5; high dose, 1.17+/-0.41; p<0.05 for both doses). A reduction in the percentage of infarct volume (low dose, 22.9+/-8.9%, p=0.002; high dose 7.6+/-3.4%, p<0.001) was seen when compared to the controls (infarct size, 54.2+/-9.0%; neurobehavior score, 2. 67+/-0.52). Treatment with TPM at the higher dose induced more neuroprotection than that at the lower dose (p<0.05). Thus, treatment with TPM resulted in a dose- and use-dependent neuroprotective effect, when used 2 h after MCA embolization in a rat model of focal ischemia.

Topics: Animals; Anticonvulsants; Brain Ischemia; Cerebral Arteries; Fructose; Hemorrhage; Intracranial Embolism and Thrombosis; Male; Rats; Rats, Wistar; Topiramate