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. ()
The patient was a 9-month-old male with a past medical history significant for in utero drug exposure and mild oral aversion, who had otherwise been reportedly well. The day prior to his initial presentation, he had been swimming with his family and was put down for a nap at 1600. Family checked on him at 2100 hours due to not waking up for dinner but found him sleeping and attributed his increased fatigue to his increased activity throughout the day. At 0700 hours the next day, family was still unable to wake the child. He was taken to the nearest emergency department, where his initial vitals were significant for hypoxemia, with oxygen saturation of 77% on room air and mild hypothermia with axillary temperature of 36.2°C. His physical exam was notable for lethargy and decreased level of arousal without external physical exam findings concerning for apparent injury or infection. Labs were significant for hypoglycemia (30 mg/dL), but his mental status did not improve with glucose supplementation. A head CT was performed, and he was found to have bilateral cerebellar hemisphere hypoattenuation with acute swelling on computed tomography (). The presumed diagnosis at the time was acute stroke of unknown etiology, with the possibility of prolonged hypoglycemia and subsequent hypoxia contributing. He was flown to the closest pediatric tertiary care center and admitted to the Pediatric Intensive Care Unit (PICU) for close neurological monitoring and further evaluation.