ABSTRACT
In May 2006, a 72-year-old man with acute myelogenous leukemia (M4Eo) was admitted to our hospital. He had been receiving antiandrogen treatment for prostate cancer (after an operation in 1998) and treatment for diabetes mellitus. He received chemotherapy according to the JALSG GML200 protocol, which led to complete remission; however, in January 2007, his leukemia recurred. CAG combination chemotherapy also resulted in complete remission by May 2007. In August 2007, he developed multiple liver tumors, abdominal pain, and fever. Contrast-enhanced computed tomography revealed hypovascular tumors in both early and delayed phases. Angiography showed ring-like tumor staining and a massive tumor, similar to those seen in metastatic hepatocellular carcinomas (HCCs). He eventually died because of aggressive enlargement of liver tumors during the following month accompanied by the simultaneous recurrence of leukemia and unsuccessful embolization of the hepatic artery. Autopsy specimens showed fibrosis and considerable iron deposition in the liver, suggested secondary hemochromatosis due to transfusion. We also detected multiple moderately differentiated primary HCCs. Secondary hemochromatosis, androgen imbalance, and humoral factors from leukemic cells were believed to be the causes of the rapid onset and development of HCCs.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Hepatocellular , Leukemia, Myeloid, Acute/drug therapy , Liver Neoplasms , Neoplasms, Second Primary , Aclarubicin/administration & dosage , Aged , Androgen Antagonists/therapeutic use , Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Carcinoma, Hepatocellular/etiology , Cytarabine/administration & dosage , Fatal Outcome , Granulocyte Colony-Stimulating Factor/administration & dosage , Hemochromatosis/etiology , Humans , Liver Neoplasms/etiology , Male , Prostatic Neoplasms/therapy , Time FactorsSubject(s)
Hemolytic-Uremic Syndrome/therapy , Adult , Humans , Male , Plasma Exchange , Renal DialysisABSTRACT
OBJECTIVES: It has been known that cervical dystonia develops secondarily to spinal cord injuries as secondary dystonia. However, little is known about the pathophysiological mechanism. PATIENTS AND METHODS: We examined motor and sensory conduction in six patients with symptomatic cervical dystonia by transcranial magnetic stimulation (TMS). All of the patients exhibited unilateral head rotation. They had symptoms corresponding to cervical myelopathy and felt discomfort in the neck, shoulders or arms before involuntary movement occurred. RESULTS: Although the overall central motor conduction time (CMCT) was not different from that of normal controls, contralateral CMCT was significantly delayed compared to ipsilateral CMCT (p<0.05). The results of somatosensory evoked potential study demonstrated that contralateral central conduction time (CCT) was not significantly different from ipsilateral CCT. CONCLUSION: These findings indicate that there is a selective interference with the contralateral corticospinal tract in patients with symptomatic cervical dystonia.
Subject(s)
Cervical Vertebrae/innervation , Evoked Potentials, Motor/physiology , Motor Cortex/physiopathology , Neural Conduction/physiology , Spinal Cord Compression/diagnosis , Spinal Stenosis/diagnosis , Torticollis/diagnosis , Adult , Aged , Dominance, Cerebral/physiology , Evoked Potentials, Somatosensory/physiology , Female , Humans , Male , Middle Aged , Pyramidal Tracts/physiopathology , Reaction Time/physiology , Reference Values , Signal Processing, Computer-Assisted , Spinal Cord/physiopathology , Spinal Cord Compression/physiopathology , Spinal Stenosis/physiopathology , Torticollis/physiopathology , Transcranial Magnetic StimulationABSTRACT
Paraneoplastic neurological syndromes are frequently associated in patients with small cell lung cancer (SCLC) and antineuronal antibodies are involved in the autoimmune mechanism. Multiple syndromes are sometimes complicated in a single patient with SCLC. However, little is known about non-SCLC-associated neurological manifestations. We report two patients with complicated paraneoplastic neurological syndromes. Patient 1 showed paraneoplastic limbic encephalitis (PLE), paraneoplastic sensory neuropathy (PSN) and Lambert-Eaton myasthenic syndrome (LEMS) associated with SCLC. Patient 2 developed opsoclonus-ataxia and probable PLE associated with non-SCLC. Analysis of various antineuronal antibodies revealed that anti-Hu and P/Q-type voltage-gated calcium channel (VGCC) antibodies were positive in Patient 1 but any antibodies were not in Patient 2. Brain MRI demonstrated high intensity signals in temporal lobes particularly on fluid-attenuated inversion recovery (FLAIR) or diffusion-weighted images. These findings suggest that complicated paraneoplastic neurological syndromes occur in non-SCLC as well as SCLC and that unidentified antineuronal autoantibodies may underlie the pathophysiology.
