Mena I, Giombetti R J, Miller B L, Garrett K, Villanueva-Meyer J, Mody C, Goldberg M A
Division of Nuclear Medicine, UCLA School of Medicine, Harbor-UCLA Medical Center, Torrance 90509, USA.
NIDA Res Monogr. 1994;138:161-73.
In summary, these data suggest that widespread primary or secondary cerebral vasoconstriction is common in patients with neurological complications from cocaine. In most patients, SPECT showed wide-spread hypoperfusion in regions that had no clear clinical significance (e.g., the periventricular area). In many, the SPECT was performed more than 24 hours after the onset of neurological symptomatology. These findings raise several questions. It has been assumed that these SPECT changes in patients with acute neurological symptoms are temporary, although it will be important to determine whether these areas of hypoperfusion persist after symptoms have abated. Recently, Holman and colleagues (1991) found multifocal and deep areas of hypoperfusion with SPECT in 16 of 18 patients with a history of chronic cocaine abuse. Although most of the subjects tested positive for cocaine, several had abstained from cocaine use for weeks prior to the study. All 18 subjects had neuropsychological deficits, 13 mild and 5 moderate. Similarly, Pascual-Leone and colleagues (1991) have shown that CT scan atrophy strongly correlates with the duration of cocaine abuse, suggesting that brain injury may occur with continued use of cocaine. It is the authors' concern that cocaine abuse might produce permanent changes in cerebral perfusion. In conclusion, brain SPECT was found to be a useful procedure in the evaluation of acute cocaine intoxication. Brain SPECT revealed focal cortical lesions not seen on head CT or MRI, which corresponded to clinical deficits. In addition, [99mTc]HMPAO brain SPECT had a characteristic scalloped appearance, and this may be a marker for acute intoxication with cocaine. This study further supports the contention that cocaine causes neurological disease by its vasoconstrictive action.
总之,这些数据表明,在患有可卡因所致神经并发症的患者中,广泛的原发性或继发性脑血管收缩很常见。在大多数患者中,单光子发射计算机断层扫描(SPECT)显示在无明确临床意义的区域(如脑室周围区域)存在广泛的灌注不足。许多患者在出现神经症状后24小时以上才进行SPECT检查。这些发现引发了几个问题。尽管确定症状缓解后这些灌注不足区域是否持续存在很重要,但一直以来人们都认为急性神经症状患者的这些SPECT变化是暂时的。最近,霍尔曼及其同事(1991年)发现,在18名有慢性可卡因滥用史的患者中,有16名通过SPECT检测出多灶性和深部灌注不足区域。尽管大多数受试者可卡因检测呈阳性,但有几名受试者在研究前几周已戒除可卡因。所有18名受试者都有神经心理学缺陷,13名轻度,5名中度。同样,帕斯夸尔 - 莱昂内及其同事(1991年)表明,CT扫描显示的脑萎缩与可卡因滥用的持续时间密切相关,这表明持续使用可卡因可能会导致脑损伤。作者担心可卡因滥用可能会导致脑灌注发生永久性变化。总之,发现脑SPECT在评估急性可卡因中毒方面是一种有用的检查方法。脑SPECT显示出头部CT或MRI未发现的局灶性皮质病变,这些病变与临床缺陷相对应。此外,[99mTc]六甲基丙二胺肟(HMPAO)脑SPECT有特征性的扇形外观,这可能是可卡因急性中毒的一个标志。这项研究进一步支持了可卡因通过其血管收缩作用导致神经疾病的观点。