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G Galassi

Publications and source records attributed to G Galassi.

62 records · Page 4Linked to original sources
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[Comparative study with a closed sequential design between iopronic and iocetamic acid in oral cholecystocholangiography with radiograms in short and standard times. Laboratory evaluation of hepatic function (author's transl)].

In a comparative study with a closed sequential design iopronic acid has shown to have an opacification power in short times (3 to 4 hours after administration) much higher than iocetamic acid. The opacification of gall bladder and choledochus at 10 to 12 hours after administration has always resulted higher for iopronic acid. Laboratory examinations (total bilirubinaemia, SGOT, SGPT) have not shown any liver damaging effect due to the administered oral cholecystographic agent. Both contrast media, finally, have not caused side effects worth a particular remark at the dosage of 4.5 g.

Administration, Oral↗
PubMedDate not supplied

[Computerized tomography in cerebellar atrophy].

Among 5680 patients who had CT cranial scans at the Radiological Service of the Hospital of Pordenone we selected by their histories and clinical findings and CT images 31 patients showing the signs of a cerebellar atrophic process. We compared CT scans with clinical symptoms; we found a correlation in 71% among CT abnormalities and clinical findings; in 22.5% CT showed an infratentorial atrophy, but clinical symptoms were absent; in 6.5% the CT scans were normal, although was present a cerebellar syndrome. We conclude that CT is an important and significative method in the diagnosis of posterior fossa degeneration, taking so the place of pneumoencephalography.

Alcoholism↗
PubMedDate not supplied

Leptomeningeal carcinomatosis presenting as progressive multineuritis: clinical, pathologic, and MRI study.

Two patients developed a persistent illness characterized clinically and electrophysiologically by asymmetric involvement of spinal roots, of cranial and peripheral nerves. In the first case the disease was not discovered clinically but only after autopsy. The primary neoplasm remained undetected at autopsy. There was profound infiltration of the leptomeninges by tumor cells with features of metastatic adenocarcinoma. In the second patient onset of neurological symptoms occurred 16 years after surgery for breast cancer, which may be reasonably considered the primary malignancy-CSF cytology was positive only in the second patient in whom Gd-DTPA MRI supported the diagnosis. Our cases demonstrate that diagnosis in leptomeningeal carcinomatosis may be a challenging clinical problem.

Carcinoma↗
PubMedDate not supplied

Motor neuron disease and HIV-1 infection in a 30-year-old HIV-positive heroin abuser: a causal relationship?

Although human retroviruses seem plausible agents of motor neuron diseases, there are only few reports of patients infected by the human immunodeficiency virus, with documented motor neuron disorder. That retroviral infections may cause motor neuron pathology by various mechanisms in animals and humans is known. Neurological symptoms potentially attributed to damage of lower motor neurons are often described during the course of HIV-1 infection and AIDS, however, it is often difficult to establish whether the disorder is primarily affecting the perikarya of lower motor neurons, or whether it is due to a focal proximal axonopathy, or to a dying-back process. We report a 30-year-old heroin abuser, HIV-1 positive, who presented a rapidly progressive limb weakness, muscle wasting, and bulbar signs, in absence of sensory loss of cerebellar and pyramidal signs. Imaging studies were negative. CSF showed increased protein content, negative cytology, and no oligoclonal bands. Serum protein electrophoresis, urinary heavy metal, and viral researches were negative. CD4 cells were counted 340 mm3 with a CD4-CD8 ratio equal to 0.4. Electrophysiology showed acute and chronic neurogenic changes, confirmed by muscle biopsy. Conduction studies along motor and sensory nerves fell within normal range. Biopsy of sural nerve revealed mild myelinated and unmyelinated fiber loss, occasional degeneration and regeneration, unremarkable inflammation. Despite treatment with AZT, zalcitabine, and steroids, the patient died after 3-month illness. Neuropathology showed normal cortical cell Betz's, and hemispheric white matter. Brain stem motor nuclei (inferior olival, dorsal motor of the vagus, hypoglossal) showed atrophy and intracytoplasmatic lipofuscin accumulation. Vacuolization, central chromatolysis, and neuronophagia were rarely seen. As associated pathology, in the fourth ventricle there were two small subependymal foci of demyelination, with reactive astrocytes and vascular proliferation. A possible crucial role of the HIV-1 infection in the development and progression of our patient's illness is considered in view of the known altered immunity proved in MND and ALS cases.

Acquired Immunodeficiency Syndrome↗