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Biomedical subjects

K Susuki

Publications and source records attributed to K Susuki.

25 records · Page 2Linked to original sources
PubMed2000

Epidural compression of the cauda equina caused by vertebral osteoblastic metastasis of prostatic carcinoma: resolution by hormonal therapy.

A 59 year old man with prostatic carcinoma developed epidural compression of the cauda equina caused by bony expansion from a vertebral osteoblastic metastasis. For medical reasons he could not undergo radiation or surgery. Hormonal therapy alone relieved his low back pain and restored ambulation and urinary function. Postmyelography CT showed that the bony expansion from the vertebra had completely disappeared after treatment. This is the first report of remarkable improvement due to hormonal therapy alone.

Bone Neoplasms↗
PubMed1999

Encephalopathy in scleromyxedema.

The authors monitored CSF findings for over 5 months in a patient with a fatal case of scleromyxedema and two episodes of encephalopathy. During both encephalopathy episodes, CSF protein and immunoglobulin G (IgG) levels were elevated without an increased IgG index or IgG synthesis rate. A CSF-dominant increase in the concentration of interleukin-6 (IL-6) also was noted during encephalopathy. These findings suggest a disruption of the blood-brain barrier and that IL-6 may play some role in mediating the encephalopathy. OFF

Brain Diseases↗
PubMed1999

[Chronic sensory ataxic neuropathy associated with IgM antibody against b-series gangliosides including GD1b].

We described a 62-year-old man with a 10 years history of chronic sensory ataxic neuropathy. His laboratory investigations revealed elevated serum IgM with IgM kappa paraproteinemia, IgM antibody against b-series gangliosides including GD3, GD2, GD1b, GT1b, GQ1b, GQ1b alpha, and high titer of cold agglutinin. The clinical and serological features in our patient were compatible with the diagnosis of CANOMAD (chronic ataxic neuropathy with ophthalmoplegia, M-protein, agglutination, and disialosyl antibodies), proposed by Willison et al. IgM antibody against b-series gangliosides including GD1b appeared to play an essential role in developing autoimmune sensory ataxic neuropathy.

Ataxia↗
PubMed1998

[Guillain-Barré syndrome with nerve conduction blocks at multiple common entrapment sites that rapidly disappeared after plasmapheresis].

Nerve conduction blocks (NCBs) in Guillain-Barré syndrome (GBS) are frequently found at the distal terminals, proximal segments, and common entrapment sites of peripheral nerves. NCBs at distal terminals and proximal segments are considered to be due to vulnerability of the sites to the humoral factors of GBS because of relative blood-nerve barrier deficiencies. In contrast, it is not clear whether NCBs at common entrapment sites in GBS are due to a vulnerability to humoral influences or to direct mechanical compression injuries. We report a case of a 22-year-old man with GBS. His electrophysiologic examination revealed NCBs at multiple common entrapment sites. All conduction blocks rapidly disappeared after plasmapheresis, in parallel with clinical improvement. The patient was ambulatory throughout the clinical course, suggesting that his common entrapment sites remained free from compression injuries. Rapid improvement by plasmapheresis suggested that there were no demyelinative histologic changes in the NCB sites. Such NCBs may be caused by some humoral factor that is removed by plasmapheresis. Therefore, the common entrapment sites in our patient may have been especially vulnerable to the humoral factor of GBS.

Adult↗
PubMed1988

Antinociception and physical dependence produced by [D-Arg2] dermorphin tetrapeptide analogues and morphine in rats.

1. The antinociceptive effects of [D-Arg2] dermorphin tetrapeptide analogues, H-Tyr-D-Arg-Phe-Gly-NH2 and H-Tyr-D-Arg-Phe-beta-Ala-OH when administered subcutaneously (s.c.) in rats were measured by the tail-flick test. In addition, the appearance of typical withdrawal signs upon cessation of administration or on subsequent treatment with naloxone were measured after chronic administration of either peptide or morphine. 2. The dose of peptides and of morphine in the physical dependence test was determined from the AD50 to inhibit the tail-flick test in rats. Doses from 4 to 64 times the AD50 doses were employed in the s.c. administration schedules. 3. The intensity of the antinociception induced by either peptide was greater than that produced by morphine. Moreover, the antinociception induced by the peptides was of much longer duration than that produced by morphine. 4. Abrupt withdrawal after chronic administration of either peptide produced only slight loss of body weight. In contrast, morphine withdrawal produced sharp loss of body weight. 5. Naloxone precipitated withdrawal signs after chronic administration of either peptide were less intense than those after chronic morphine. 6. These results suggest that the antinociception produced by these peptides is more intense and of longer duration than that produced by morphine. It is also interesting to note that the physical dependence produced by these peptides is less marked than that produced by morphine.

Analgesics↗