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. 2011 Feb 17;2011:865319. doi: 10.4061/2011/865319

Table 1.

Summary of clinical and MRI data from the different reports (EDTA: ethylenediaminetetraacetic acid, GP: globus pallidus, GPi: internal part of globus pallidus, NCh: head of caudate nucleus, PAS: para-aminosalicylic acid, SI: signal intensity, SN: substantia nigra, SNr: reticular part of substantia nigra, STN: subthalamic nucleus, y: years).

Publication No. of the subjects Age (y) Time to the symptoms Initial symptoms MRI findings Treatment Outcome
Levin 2005 [33] 21 15–36 (21 ± 5.8) 3–14 (6.8 ± 4.9) months Disorders of speech (33%) and gait (29%), fatigue (29%), bradykinesia (14%), affective symptoms (19%) T1 bilateral symmetric SI in GPi, SNr—18 (86%); no correlation with duration of usage, dosage nor severity of the symptoms EDTA, l-dopa, clonazepam, amantadine Spontaneous regression of the symptoms—29%, worsening—33% even after 4 y abstinence
Sikk et al. 2007, 2010 [14, 34] 4 (case reports) 24–42 6 months–8 y Gait disorder—2, hypophonia—2 T1 SI increase in GP, putamen, NCh—2 cases; decrease of SI in the same areas—1 Not reported Initial improvement then stable—1, stable still using—1, slow progression of the symptoms—2
De Bie et al. 2007 [19] 1 (case report) 36 Not exactly reported, possibly 4–16 months Decrease of libido; sleepiness, slowness Symmetric SI increase in GP, SN dentate nucleus, and pontine tegmentum Pramipexole, selegiline, l-dopa No improvement
Sanotsky et al. 2007 [15] 6 (case reports) 23–45 2 months–1 y Speech and gait disorder—1, plus bradyphrenia or depression—2, slowness—2, hyperthermia—1 Striking bilateral SI increase of lentiform nucleus, SN, dentate nucleus EDTA, cerebrolysin, amantadine, l-dopa Mild to moderate improvement—4, no improvement—2
Meral et al. 2007 [35] 2 (case reports) 21 and 32 Unknown, 4 months Bradykinesia, gait and speech disorders Bilateral SI increase in GP. After withdrawal of injections, improvement of MRI in case 2 Not reported No improvement
Stepens et al. 2008 [17] 23 37.5 ± 6.5 5.8 ± 4.5 y Gait disturbance—20 (87%), hypophonia—3 (13%) T1 SI increase in GP—all 10 active users, in SN—9; former users had lesser degrees of change (SI increase in GP—11, SN—2, anterior midbrain—3) L-dopa in 3 patients No substantial improvement in 13 subjects after withdrawal for 2–6 y
Selikhova et al. 2008 [16] 13 18–46 (29.9) 8.5 ± 3.2 months Loss of balance—7, slurred speech—4, mood disorders—2 T1 SI increase mostly in GPi,—all; other frequently involved structures—STN, SNr, putamen L-dopa, amantadine, EDTA, Significant residual deficit; delayed progression in some cases
Colosimo and Guidi 2009 [18] 1 (case report) 28 2 y Gait and speech disturbance, mental slowness, generalized fatigue Repeated MRI normal Not reported Some deterioration of motor signs
Yildirim et al. 2009 [36] 1 (case report) 29 9.5 y since start of abuse, 5 y abstinence Gate disturbance, mood disorders Normal Piracetam, carbamazepine, fluoxetine, l-dopa Gradual worsening over time
Varlibas et al. 2009 [37] 3 (case reports) 15–19 2–6 y Postural instability, face and limb dystonias, tremor, dysphonia, dysarthria, bradykinesia Bilateral symmetric SI increase in dentate nucleus, white matter of cerebellum, GP and putamen EDTA, PAS, l-dopa No improvement