Nicotine for the treatment of Tourette's syndrome.

Recent evidence has demonstrated that nicotine may obtund the symptoms of Tourette's syndrome (TS). TS is a neuropsychiatric disorder characterized by motor and vocal tics, obsessions and compulsions, and frequently with impulsivity, distractibility, and visual-motor deficits. While neuroleptics, such as haloperidol, are most effective for treatment of the motor and vocal tics of TS, these medications have many side effects. In this article, we review the evidence, consistent with findings in animals, that administration of nicotine (either 2 mg nicotine gum or 7 mg transdermal nicotine patch) potentiates the therapeutic properties of neuroleptics in treating TS patients and that a single patch may be effective for a variable number of days. These findings suggest that transdermal nicotine could serve as an effective adjunct to neuroleptic therapy for TS.

Nicotine potentiates the effects of haloperidol in animals and in patients with Tourette syndrome.

Nicotine was found to markedly potentiate haloperidol-induced hypokinesia in rats. Nicotine alone was without effect. Subsequently, concurrent administration of 2 mg nicotine gum to 10 Tourette syndrome patients being treated with haloperidol produced a substantial decrease in tics and improvement of concentration and attention span. Nicotine gum alone was without effect. While 80% of children showed improvement with nicotine gum, 70% completely discontinued the gum because of side-effects, primarily involving nausea and bitter taste. Nicotine may prove useful for treating other neuroleptic responsive disorders, such as schizophrenia and Huntington's disease.

Hypoxic brain and heart injury thresholds in piglets.

Both heart and brain are at risk for damage from asphyxia. However, these 2 organs' relative injury-thresholds have remained poorly defined. The present study using 16 anesthetized newborn piglets attempts to separate brain and heart damaging exposures from those that leave these organs unaffected. The hypoxic exposure (mean PaO2 = 3.6 +/- 0.6 kPa (27 mmHg) lasted for an average duration of 40 minutes and was associated with hypotension less than 4.7 kPa (35 mmHg) MABP. For brain damage assessment, 9 piglets that survived greater than 12 hours following resuscitation permitting histologic evaluation were used. For heart outcome assessment, those piglets that developed a postexposure, secondary hypotension to less than 4.7 kPa (35 mmHg) were compared to those without excluding 3 with uncertain cause of death. BRAIN-RESULTS: Six piglets remained brain intact while 3 exhibited brain edema and diffuse neuronal damage. The damaged animals' exposures differed from those that remained brain intact in sustaining significantly lower lowest MABPs (1.6 +/- 0.1 vs 3.3 +/- 0.4 kPa (12 vs 25 mmHg] and longer durations of MABP below 3.3 kPa (25 mmHg): 6 vs 1 min. and below 2.7 kPa (20 mmHg): 4 vs 0 min. HEART-RESULTS: Six of 13 animals developed marked delayed post-exposure hypotension requiring 5 to be killed prior to complete cardiovascular collapse. The only significant difference observed during exposure differentiating the two outcome groups (blood pressure maintenance vs cardiogenic shock) was the latter's more marked systemic acidosis (lowest mean arterial blood pH: 6.61 +/- 0.10 vs 6.91 +/- 0.10). These results suggest the brain is at risk for damage during hypoxia only when accompanied by an extreme lowering of blood pressure and the heart when accompanied by a severe acidosis. Further, the heart and brain need not both be damaged by the same hypoxic exposure. Contrary to common belief, the brain is not readily damaged from hypoxia alone absent marked circulatory changes.