A patient with acute monocytic leukaemia and gross ocular involvement successfully treated with local irradiation is described. Leukaemic infiltration of the sclera developed at a time when the patient appeared to be in haematological remission. Despite the frequency of extramedullary disease in monocytic leukaemia the diagnosis of monocytic sarcoma may be very difficult.

Four cases of C.G.L. in which banding of the Ph1 chromosome was performed were found to have variation from the usual 9/22 translocation pattern. All 4 cases showed a rearrangement involving at least 3 chromosomes, 2 of which were a9 and a22. One of these cases had in addition an XYY karyotype in the bone marrow.

2 cases of acute lymphoblastic leukaemia characterised by the presence of cytoplasmic inclusions morphologically similar to azurophil granules are described. Azurophil granulation of blasts is one of the cardinal features which differentiate acute myeloid from acute lymphoblastic leukaemia. Although such granulation of lymphoblasts has caused diagnostic confusion in the past, we found that the granules could be distinguished from myeloid azurophil granules both morphologically and by their characteristic cytochemical staining reactions. They were negative for peroxidase/sudan black and chloroacetate esterase, but gave coarse scattered granular positivity for both acid phosphatase and alpha‐naphthyl acetate esterase. Both the electron microscopic appearance of the granules and their cytochemical staining reactions suggested that they were lysosomes. Granular ALL does not appear to be associated with any morphological subtype or karyotype; but is strongly associated with the common ALL phenotype. Its prognostic significance remains uncertain. It occurs more frequently than the small number of previous reports might suggest and, given the potential for misdiagnosis, should be more widely recognised.

The sheep lung-lymph model has proven to be a valuable research tool. Preparing this model can be time consuming and may cause considerable trauma to the animal. The standard procedure of Staub et al., the only other published technique, requires three thoracotomies performed on three separate occasions. The objective of this study is to develop and evaluate a less traumatic and time-consuming surgical protocol for preparing the lung-lymph model. This technique enables us to cannulate the efferent lymph duct draining the lung, divide the caudal mediastinal lymph node, and catheterize the left atrium with one thoracotomy. The modified approach, along with some minor changes in aftercare, enables us to have a success rate of over 70% with an average patent flow of 8 days (range 3-21 days) and saves time and surgical trauma to the animal.

enth day after admission. At the time of discharge, she continued to complain of extremity pain. Neurologic examination at 3week follow-up was normal although she continued to complain of extremity pain. EMG did not show any significant abnormality except for slightly prolonged distal sensory latencies in the left median nerve. Repeat brain MRI at 6 weeks showed nearly complete resolution of the supratentorial white matter and cerebellar abnormalities (figure, C). At a recent follow-up, the patient's symptoms of painful hands and feet persisted with some response to nocturnal amitriptyline, and examination remained normal. Repeat EMG was normal.Discussion. Animal studies in dogs have shown Purkinje cell damage after prolonged administration of high doses of metron i d a~o l e .~ Labeled metronidazole has been localized in the rat brain, spinal cord, and dorsal root ganglia, and there is radioisotope activity in RNA of the nervous t i~s u e .~ Metronidazole or its metabolites may bind to neuronal RNA and inhibits protein synthesis, resulting in axonal degeneration. Histologic section of rat brain after treatment with 800 m g k g of metronidazole has shown symmetric lesions in the ventricular and cochlear nuclei as well as in the cerebellar roof nuclei, colliculus, and superior olive.6 These lesions were histologically similar to those in Wernicke's encephalopathy in humans. Metronidazole crosses the blood-brain barrier in humans. ' Our patient had symptoms attributable to metronidazole toxicity, including dizziness, ataxia, confusion, nausea, vomiting, joint pain resembling serum sickness, and peripheral neuropathy. All of the symptoms cleared on discontinuation of the medication except for dysesthesia in the extremities. Since these dysesthesias may be due to degeneration of sensory fibers, they may persist for several months until regeneration of these fibers can occur.The MRI lesions involving supratentorial white matter and the deep cerebellar nuclei account for the patient's encephalopathy and cerebellar dysfunction, including vertigo. As the MRI findings were reversible, they were not due to a demyelinating process. A more likely explanation is that the acute toxic insult produces axonal swelling with increased water content, resulting in T, prolongation. Wilson et a17 reported a case of reversible MRI changes due to cyclosporin A toxicity where pathologic examination showed swollen myelin sheaths with only a few minute demyelinating lesions. An alternative explanation for the MRI signal changes is vascular spasm that might produce mild reversible localized ischemia.The differential diagnosis of multifocal, fairly symmetric lesions involving both white and gray matter without significant mass effect in MRI must include demyelinating diseases as well as metabolic infectious and inflammatory processes in addition to drug toxicity. Multiple sclerosis and acute disseminated encephalomyelitis could account for the MRI findings, but involvement of gray matter, normal CSF, and temporal profile make these possibil...