Cocaine snorting may induce ocular surface damage through corneal sensitivity impairment.

PURPOSE: Cocaine abuse may cause severe ischemic and necrotic tissue damage in several organs, including the eye. However, the cornea is an avascular tissue relying on sensitive nerves for its trophic support, and the pathogenesis of cocaine-induced corneal lesions is unclear. In this study, we aimed to investigate if corneal sensitivity, ocular surface, and tear function are damaged by habitual cocaine snorting. METHODS: Ocular examination, corneal sensitivity, and tear function testing were carried out in 48 cocaine addicts, and in 22 heroin addicts and 30 drug-free age/sex-matched individuals who served as controls. We also performed corneal confocal microscopy, conjunctival impression cytology, and tear sample collection to evaluate corneal and conjunctival morphology, and the presence of cocaine in tears. Statistical analysis was performed to compare groups and to correlate clinical findings with anamnestic data on cocaine use. RESULTS: We observed decreased corneal sensitivity in 26 cocaine addicts, and neurotrophic keratitis in six of them, with corneal damage, absence of symptoms, reduced tear production, and prolonged interblink-time. No significant changes in ocular surface parameters including corneal sensitivity were observed in heroin addicts. The major risk factors for developing cocaine-induced neurotrophic keratitis appeared to be duration and frequency of drug abuse. CONCLUSIONS: A complete ophthalmic evaluation including corneal sensitivity testing should be planned for an optimal management of cocaine addicts, even in the absence of ocular symptoms, to reduce the risk of corneal lesions and consequent vision impairment. Sensory nerve damage should also be evaluated in cocaine-induced lesions of other organs.

Headache in chronic cocaine users: A cross-sectional study.

BACKGROUND: Headache is one of the most common symptoms after cocaine use. METHODS: We investigated headache frequency and characteristics and the correlation between headache and acute cocaine intake in a cross-sectional study in a consecutive series of chronic cocaine users. RESULTS: Participation rate was 94.1%. Of the 80 subjects enrolled, 72 (90%) reported current headaches, in most cases migraine or probable migraine without aura. Of these 72, 29 (40.3%) had a headache history, whereas 43 (59.7%) reported de novo headache after beginning to use cocaine. After acute cocaine use, a large percentage of users reported headache attacks: 86.2% of previous headache sufferers (migraine or probable migraine without aura in all cases) and 93% of de novo headache sufferers (migraine/probable migraine without aura = 35; episodic tension-type headache = three patients; cocaine-induced headache= two patients). Most subjects reported that when they used cocaine headaches worsened. CONCLUSION: Chronic cocaine use frequently seems to worsen or induce headache with migraine or migraine-like characteristics, probably owing to a serotoninergic and dopaminergic system impairment. In headache sufferers, especially those with migraine headaches, clinicians should enquire into possible cocaine use.

Atypical antipsychotics and polydipsia: a cause or a treatment?

Primary polydipsia (PP) is a frequent complication that affects many chronic schizophrenic inpatients. Due to possible lethal consequences, for example, hyponatremia, coma and death, it's fundamental for the physician achieving early diagnosis and treating this condition. The first step is identifying polydipsia by clinical, biochemical and pharmacological means. Nowadays, the pathophysiology of PP remains unclear, and this limits the possibility of detecting an appropriate drug treatment. Typical antipsychotics have been associated to a worsening of polydipsic behavior, while more recently atypical antipsychotics have been reported as being useful. However results are still mixed and controversial. It appears that risperidone and olanzapine are not clearly effective; clozapine may improve symptoms, although it is difficult to manage from a therapeutic point of view; quetiapine has been poorly studied so far, nonetheless it has given interesting results. Through a case study analysis, this report presents a brief, yet selective, overview of the current state of psychopharmacology in the treatment of PP with atypical antipsychotics in schizophrenia.

Combining an SSRI with an anticonvulsant in depressed patients with dysphoric mood: an open study.

BACKGROUND: Several patients with unipolar depression present with prominent dysphoric mood. We aimed at examining the effectiveness of the combination of an SSRI with an anticonvulsant in such patients. METHODS: Thirty-five newly admitted outpatients with substantial anger, irritability, aggressiveness or hostility who were diagnosed a DSM-IV unipolar depressive disorder were rated on the Hamilton Depression Rating Scale (HDRS), the Clinical Global Improvement (CGI) scale, and a scale for the rapid dimensional assessment (SVARAD), were prescribed an SSRI and an anticonvulsant (usually valproate), and were followed up for 12 weeks. Repeated measures analysis of variance was used to test for within-subject changes in scale scores over time. RESULTS: Thirty-two and 23 patients attended the follow-up visits 4 and 12 weeks later, respectively. Significant decreases (p < .001) were observed in HDRS total score, HDRS and SVARAD anxiety factors, HDRS and SVARAD core depression factors, and SVARAD anger/irritability factor. Adjusting for age or gender did not change the results. Most patients (82%) were rated as improved or much improved on the CGI. CONCLUSION: Although our study has several limitations, we observed a remarkable improvement in most unipolar depressed outpatients with dysphoric mood treated with an SSRI and an anticonvulsant. The effectiveness of anticonvulsants might be linked to their action on symptoms of aggression and behavioural activation.