A case of follicular lymphoma associated with paraneoplastic cerebellar degeneration.

Paraneoplastic neurological disorders (PND) are neurological effects of malignancy that are recognized as immune-mediated disorders caused by aberrant expression of a tumor antigen that is normally expressed in the nervous system. We report a case of cerebellar ataxia which turned out to be paraneoplastic cerebellar degeneration, a subtype of PND that develops cerebellar symptoms, that was caused by follicular lymphoma. After chemotherapy, the patient attained sufficient improvement of cerebellar symptoms along with complete remission of lymphoma. Paraneoplastic cerebellar degeneration should be recognized as a rare complication of lymphoma as it is important to start proper treatment before the neurological symptoms become irreversible.

[A case of myeloradiculitis as a complication of visceral larva migrans due to Ascaris suum].

A 35-year-old man noticed a tingling sensation and subsequent slight weakness in the distal part of the left lower extremities, which extended to the left thigh over the following 8 months, when he developed a urinary disturbance. He was admitted to a local hospital and diagnosed as having myelitis, because of the presence of a gadolinium (Gd)-enhanced lesion in the lumbar spinal cord corresponding to the tenth thoracic vertebra (Th10) level. The symptoms disappeared along with some residual sensory disturbance following intravenous administration of 1 g of methylprednisolone (IVMP) for 3 days. However, 4 months later, the patient gradually developed gait disturbance, dysuria, impotence, and fecal incontinence, and was admitted to our hospital in May 2001. A neurological examination revealed the presence of myeloradiculopathy causing a slight weakness in the left hamstring muscles, with positive Babinski and Lasegue signs on the same side. In addition, deep tendon reflexes were absent in the 4 extremities and vibration sense was moderately decreased in the lower extremities, though the results of electrophysiological tests of motor and sensory nerves were normal. A magnetic resonance imaging (MRI) study showed a Gd-enhanced lesion in the spinal cord at the Th8-9 vertebrae level, which was 1 to 2 vertebrae above the initially detected lesion. A lumbar puncture yielded cerebrospinal fluid (CSF) containing mononuclear cells at 7/mm3 that were comprised of an increasd number of CD4+CD25+ activated helper T cells; however, no myelin basic protein or oligoclonal IgG band was present. Serological examinations were negative for the presence of collagen/vascular disorders as well as viral infection due to CMV, EBV, HSV, VZV, and HTLV-1, however, positive for specific antibodies against Ascaris suum in both serum and the CSF, confirming the diagnosis of chronic myeloradiculitis due to visceral larva migrans. The patient was first treated with a single course of a daily 600-mg dose of oral albendazole for 4 weeks, which was resulted in restoration of muscle weakness, as well as disappearance of the Lasègue sign. However, in contrast to the clinical improvement, the CSF sample obtained immediately after completing the treatment showed a worsening trend, as the CSF cell count had increased with a manifestation of marked eosinophilia and CD4+CD25+ cells were also increased. Thereafter, 3-day IVMP treatment was performed twice in cojunction with 3 courses of oral albendazole therapy for the subsequent 4 months, which resulted in normalization of all laboratory measurements concerning the CSF along with a decrement trend in serum and CSF antibody titers specific to Ascaris suum. Our results suggest that neurological involvement due to visceral larva migrans can be efficaciously treated with not only helminthic drugs but also intravenous corticosteroids.

Licorice-induced hypokalemia as a treatable cause of dropped head syndrome.

Isolated weakness of the extensor muscles of the neck is a relatively rare condition, known as "dropped head syndrome" (DHS). This paper reports the case of a patient with DHS whose symptoms resolved rapidly on supplementation with potassium and discontinuation of licorice consumption. To the best of our knowledge, there are no reports in the literature of DHS due to licorice-induced hypokalemia.