Painful Sensory Motor Neuropathy With Albuminocytological Dissociation of the Cerebrospinal Fluid as the Presenting Features of Acute Thallium Poisoning

A great variety of neurological diseases require investigation of cerebrospinal fluid (CSF) to prove the diagnosis or to rule out relevant differential diagnoses. The objectives were to evaluate the theoretical background and provide guidelines for clinical use in routine CSF analysis including total protein, albumin, immunoglobulins, glucose, lactate, cell count, cytological staining, and investigation of infectious CSF. The methods included a Systematic Medline search for the above-mentioned variables and review of appropriate publications by one or more of the task force members. Grading of evidence and recommendations was based on consensus by all task force members. It is recommended that CSF should be analysed immediately after collection. If storage is needed 12 ml of CSF should be partitioned into three to four sterile tubes. Albumin CSF/serum ratio (Qalb) should be preferred to total protein measurement and normal upper limits should be related to patients' age. Elevated Qalb is a non-specific finding but occurs mainly in bacterial, cryptococcal, and tuberculous meningitis, leptomingeal metastases as well as acute and chronic demyelinating polyneuropathies. Pathological decrease of the CSF/serum glucose ratio or increased lactate concentration indicates bacterial or fungal meningitis or leptomeningeal metastases. Intrathecal immunoglobulin G synthesis is best demonstrated by isoelectric focusing followed by specific staining. Cellular morphology (cytological staining) should be evaluated whenever pleocytosis is found or leptomeningeal metastases or pathological bleeding is suspected. Computed tomography-negative intrathecal bleeding should be investigated by bilirubin detection.

Thallium poisoning is known for its diverse manifestations and these can delay the diagnosis if a clear history of poisoning is not forthcoming. A 42 year old man presented on the third day of illness with flaccid quadriparesis and paresthesia, which were confused with Guillain-Barré syndrome. Because of associated loose motions, skin lesions, and liver and kidney dysfunction arsenic poisoning was considered. In the second week he developed ophthalmoplegia, nystagmus, and neck tremor and later developed alopecia, and thallium poisoning was suspected. His serum thallium level on the 18th day of illness was 40 980 micro g/ml. He was subjected to haemodialysis, potassium supplementation, laxatives, and B complex supplementation. He showed significant improvement after haemodialysis and at three months he was able to walk with support. At six months of follow up he was independent for activities of daily living. Severe paresthesia, ophthalmoplegia, cerebellar and extrapyramidal signs, and alopecia are highly suggestive of thallium poisoning. Haemodialysis may be effective even in the third week of poisoning.