A 25-year-old man with history of cocaine use presented to the emergency room with left-sided upper and lower limb weakness as well as sensory impairment involving the face. Symptoms evolved such that he was bed-ridden after 48 h. He had no history of previous neurological or systemic symptoms. Computed tomography (CT) of the brain showed bilateral periventricular hypodensities. CT angiography of cervical and intracranial vessels was unremarkable. An MRI study of the brain demonstrated increased FLAIR signal deep in the right and left hemispheres (Fig. ), which also displayed patchy gadolinium enhancement (Fig. ) and restricted diffusion (Fig. –). Five days after admission he developed swallowing difficulty, dysarthria, and confusion. In addition to the previously noted MRI abnormalities, repeat imaging showed new lesions in the left internal and external capsules, putamen and corona radiata, right medial pons and left cerebellar peduncle, with heterogenous gadolinium enhancement (Fig. –). The neuroradiological impression was that the lesions were most compatible with demyelinating disease. A urine screen was positive for cocaine, cannabinoids, and oxycodone, and negative for amphetamine, methadone, benzodiazepines, and barbiturates. Other investigations included the following normal or negative results: complete blood count, serum electrolytes, urea, creatinine, glucose, erythrocyte sedimentation rate, antinuclear antibodies, rheumatoid factor, perinuclear and cytoplasmic anti-neutrophil cytoplasmic antibodies (pANCA and cANCA respectively), extractable nuclear antigens, lupus inhibitor, C3, C4, CH50, urinalysis, vitamin B12, angiotensin converting enzyme level, thyroid stimulating hormone level, free T3 and T4, cortisol level, lipid profile, very long chain fatty acids, viral serology for HIV, CMV, Hepatitis A, B, and C, Lyme serology, syphilis screen, blood screen for salicylate, acetaminophen, and ethanol. Liver enzymes (AST, ALT and GGT) were mild to moderately elevated and subsequently normalized over a period of six months. Cerebrospinal fluid (CSF) results included: slightly elevated protein at 0.50 g/l (normal 0.20–0.40 g/l), normal glucose and chloride, normal total cell count (3 × 106/l), negative oligoclonal bands, normal IgG index, elevated albumin index at 9.0 (2.7–4.7), negative cryptoccocal antigen, negative cultures for bacteria and fungi, negative polymerase chain reaction (PCR) studies for CMV and HSV 1–2, and normal cytology.\nHe was treated with intravenous methylprednisolone, 1000 mg daily for five consecutive days, and subsequently underwent plasma exchange. During plasma exchange his neurological condition stabilized and he subsequently achieved good, albeit partial, recovery. At three months follow-up he had mild residual left-sided hemiplegia but was otherwise independent in activities of daily living and starting to return to work. Follow up MRI five months after presentation showed reduction in the size of lesions, no enhancement, and no new lesions (Fig. –). MRI 21 months after the initial presentation also showed no new lesions (not shown).
A 53-year-old man was admitted to the Neurology Department of Farabi Hospital (Kermanshah, Iran) with walking inability and recognition disorder. Patient history showed that he had referred to hospital with vomiting, vertigo and headache 8 months before after consumption of two sachet of levamisole (for veterinary use) which each sachet contained 1.5 gram of levamisole hydrochloride. One month later, he had been stricken by progressive walking inability and recognition disorder up to administration to our hospital. The patient had not any previous illness.\nOn neurologic examination, he was confused and did not establish a good relationship with the bystander. On mental and cognitive power examinations, using the Mini Mental State Examination (MMSE), he earned 17 points (out of a total score of 30) with no signs of meningeal irritation (such as stiffness of neck). In addition, cranial nerves were normal. The power of limbs was within normal range but deep tendon reflexes in all of four limbs had increased in conjunction with extensor plantar response and reduced abdominal skin reflex. The patient had primitive reflexes including grasp, snout and palmomental. On cerebellar examination, finger to nose test and heel to shin was impaired and the gait was ataxic.\nOn the initial laboratory tests, complete blood count (CBC), blood sugar, urea, creatinine, and liver enzymes were normal. In cerebrospinal fluid analysis, color, pressure, cells, and sugar were normal but protein was increased (69 mg/dl). Oligoclonal band (OGB) was negative.\nOn electroencephalography (EEG), bilateral paroxysmal slow waves were seen. In visual evoked potential (VEP), there was a bilaterally prolonged P100 latency. Brain magnetic resonance imaging (MRI) showed mild cerebral atrophy and multiple focal lesions distributed in periventricular and cerebellar white matter and also in pons and midbrain (). These lesions had low-signal intensity on T1-weighted images and high-signal intensity in fluid-attenuated inversion recovery (FLAIR) view and T2-weighted images.\nFollowing clinical examinations and ruling out of other causes, including infectious and vascular causes, trauma and metabolic, central nervus system (CNS) vasculitis and paraneoplastic syndromes; and according to the patient's history, the patient was diagnosed as multifocal inflammatory leukoencephalopathy following levamisole consumption. The patient did not give consent for brain biopsy.\nThe patient was treated with intravenous methylprednisolone (500 mg) every 12 hours for 7 days followed by two weeks oral consumption of the prednisolone (50 mg/day) during hospitalization. No change was noticed in cerebellar signs and gait disorder but a brief improvement was seen in mentality and cognition after 1 and 3 months. After a month of treatment, MRI did not show a reduction or remission of the lesions. ()