Journal of the Neurological Sciences 160 (1998) 180–182 Bilateral borderzone brain infarctions in association with heroin abuse Ludwig Niehaus*, Bernd-Ulrich Meyer Department of Neurology of the Charite´, Virchow Klinikum, Humboldt-University, Berlin, Germany Received 27 February 1998; received in revised form 30 June 1998; accepted 2 July 1998 Abstract A 25-year-old drug abuser who developed an unusual pattern of cerebral ischemic lesions is presented. Cerebral magnetic resonance imaging revealed bilateral borderzone infarctions which were attributed to a heroin-associated vasculitis of the basal cerebral arteries. Under probatory corticosteroid medication the mild neurological deficits completely disappeared.  1998 Elsevier Science B.V. All rights reserved. Keywords: Stroke; Heroin; Magnetic resonance imaging; Ultrasonography 1. Introduction Cerebral strokes in heroin addicts that occur in the absence of endocarditis or mycotic aneurysms are a rarely observed condition [4]. According to our knowledge, only 14 such cases clearly associated with heroin abuse have been reported [1]. Brain imaging was only performed in five of these cases (four with CT, one with MR) and showed unilateral infarctions in the territories of the middle and posterior cerebral arteries [1,3,7]. The etiology of the infarctions was attributed to microembolism or to toxic or immune vascular injury [1,3,4,7]. Here we report a case with an unusual pattern of bilateral ischemic lesions and an extraordinarily good functional recovery. 2. Case report Three days after a heroin injection, a 25-year-old unemployed worker with a history of episodic alcohol and heroin abuse developed a series of three generalized epileptic seizures. He was admitted to an intensive care *Corresponding author. Neurologische Kliniken, der Humboldt-Uni¨ Virchow Klinikum, Augustenburger Platz 1, 13353 Berlin, versitat, Germany. Tel.: 149-30-45060011; fax: 149-30-45060901. unit and the seizures promptly stopped after intravenous application of benzodiazepines. At no time were circulation or ventilation critical. Two days after admission, left hemiparesis, disorientation and mild rhabdomyolysis occurred. Rhabdomyolysis was associated with heroin toxicity [5] since no evidence of preceding muscle compression was present. While the initial CT of the brain had shown no abnormality, at this time it revealed low-density lesions in the parieto-occipital and frontal regions of both medial hemispheres. Cerebrospinal fluid showed no abnormalities. Other laboratory findings were an increased blood sedimentation rate, a slightly elevated IgE concentration (300 U / l, normal below 150 U / l) and a positive cardiolipin antibody test (16.7 U / ml; IgM, normal below 10 U / ml), while TPHA and HIV tests were negative. Skin biopsy of the thigh revealed perivascular lymphocytic infiltration. Furthermore slight macrocytic anaemia and thrombocytopenia (75 000 cells / ml) were found. Prothrombin time, partial thromboplastin time, thrombin time and fibrin concentration lay within normal range. Rheumatoid factors and antinuclear, anti-smooth muscle antibodies, were absent. Levels of circulating immune complexes lay within normal range. None of the findings, including a normal transoesophageal echocardiogram, suggested bacterial endocarditis or the heart as the source of emboli. 0022-510X / 98 / $ – see front matter  1998 Elsevier Science B.V. All rights reserved. PII: S0022-510X( 98 )00241-X L. Niehaus, B.-U. Meyer / Journal of the Neurological Sciences 160 (1998) 180 – 182 Ten days after onset of the hemiparesis T2-weighted images showed hyperintense lesions in the border zones between the territories of the anterior (ACA) and middle (MCA) cerebral arteries and posterior (PCA) and middle cerebral arteries (Fig. 1). Small circumscript areas of cortical hyperintensities in T1-weighted images indicate petechial haemorrhages (Fig. 1). No clear signal enhancement after Gd-DTPA application occurred. Three arguments support the assumption that the described mor- 181 phological changes reflect a bilateral borderzone infarction and not simply a circumscript cerebral edema: The lesions were (i) not space-occupying, (ii) restricted to the cortical and subcortical borderzones of the cerebral arteries, and (iii) associated with small cortical bleedings. Cerebral angiography showed a slight bilateral segmental narrowing of the supraclinoid internal carotid arteries and proximal segments of the MCA and ACA without concomitant occlusions of distal arteries or of the veins. Fig. 1. (A), (B) T2-weighted (SE, TR 2500 ms, TE 80 ms) brain MR images 10 days after onset of left hemiparesis in a heroin addict show bilateral hyperintensities in the border zones between the territories of the anterior and middle and the posterior and middle cerebral arteries. (C), (D) T1-weighted MR images (SE, TR 600 ms, TE 10 ms) reveal lesions with petechial gyral haemorrhages (arrows) and no enhancement after Gd-DTPA application (D). 182 L. Niehaus, B.-U. Meyer / Journal of the Neurological Sciences 160 (1998) 180 – 182 The left PCA originated from the internal carotid artery. Transcranial Doppler sonography was performed on the 6th, 14th and 21st day after onset of the symptoms. On the 6th day Doppler sonography revealed pathologically increased mean blood flow velocities with a disturbed flow pattern (high intensity of low-frequency components) in the supraclinoidal segments of both internal carotid arteries (.120 cm / s; normal mean value of 3969 cm / s, see Ringelstein [8]) and in the proximal segments of the ACA and MCA (.100 cm / s; normal mean value [8] for the ACA 50611 cm / s and for the MCA 55612 cm / s). Normal mean blood flow velocities were measured in the distal segments of the MCA (36–60 cm / s) and PCA (35 cm / s). The blood flow velocities within the extracranial internal carotid artery lay within normal range. The increased mean blood flow velocities normalized in the follow-up transcranial Doppler examinations within 3 weeks. It can be assumed, that at the time of the stroke the blood flow velocities were even higher than on the 6th day and that the initial constriction of the proximal segments of the cerebral arteries was haemodynamically relevant. These findings indicate a segmental vasospasm of basal cerebral arteries and exclude a hyperdynamic state of cerebral perfusion. Under the assumption of heroin-associated vasculitis, probatory high-dose corticosteroid medication was prescribed (initial dose, 1 g prednisolone per day) for 1 month. The hemiparesis and disorientation completely disappeared within 3 weeks. 3. Discussion Bilateral borderzone infarctions such as those in the presented case are usually explained by haemodynamic mechanisms and are described for episodes of severe hypotension [2]. Such a pathomechanism can be ruled out in the presented case, since blood pressure and oxygenation lay within normal range at admission and during the following 9 days of intensive care monitoring. The reduced diameter of the proximal segments of the basal cerebral arteries seen in the angiogram was paralleled by increased blood flow velocities in these vessels and might have caused a hypoperfusion in the watershed zones between the middle and posterior cerebral arteries and the middle and anterior cerebral arteries in which the infarctions were located. The reversible narrowing of the basal arteries could have been related to a drug-induced vasospasm or a vasculitis. The latter was suspected on the basis of slightly increased cardiolipin antibody and IgE concentrations and the lymphocytic perivascular infiltration of the skin. In other cases immunological abnormalities were also described, which were attributed to immune-mediated mechanisms of vascular injury and stroke in heroin addicts [3,7]. In these cases unilateral strokes were related to vasospasm and signs of arteritis in cerebral angiography. We propose that the seizures which occurred in the early stage of the disease are related to transient cortical ischemia rather than to heroin toxicity or alcohol withdrawal. Seizures after subcortical infarction are also a rare condition. In the SASS (Seizures After Stroke Study) only some patients with small infarcts in the corona radiata and with cortical areas of low blood flow had generalized seizures [6]. In this case of a young drug abuser, the etiology of the observed unusual bihemispheric infarctions might have been related to an autoimmune vascular process but finally remained unclear. The good functional recovery under probatory corticosteroid medication should raise the question of whether such a therapeutic regimen should be considered in patients with heroin-related strokes in the absence of indications of embolic or infectious origin. References [1] Bartolomei F, Nicoli F, Swiader L, Gastaut JL. 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