Minamata disease (organic mercury poisoning): neuroradiologic and electrophysiologic studies.

We studied 10 patients with Minamata disease (organic mercury poisoning) who have been followed for over 20 years. CT revealed a bilateral, symmetric, low-density area in the visual cortex and diffuse atrophy of the cerebellar hemispheres and vermis, especially the inferior vermis. Computerized quantitative analysis of the tremor of these patients showed a peculiar frequency of 7.075 Hz on postural tremor and 7.501 Hz on action tremor. On studies of short-latency somatosensory evoked potential, all patients showed a lack of the N20 component, the potential of the somatic sensory area.

[A quantitative analysis of ataxia in the upper limbs].

By using a transparent digitizer and a personal computer, we tried a quantitative analysis of ataxia in the upper limbs. A total of 25 upper extremities of 13 patients with spino-cerebellar degeneration (SCD) and 140 upper extremities of 70 normal volunteers were tested by two types of tasks. One was the free speed trace of a circle presented on the display (free circle), and the other was the pursuit of a target moving on a circle at a fixed speed (pursuit circle). The digitizer was put on a color display stabilized horizontally. For 1024 points with a 25 msec sampling time, the trajectory of the stylus pen was transmitted to the computer in real time. Circle diameters of 3 cm and 6 cm were selected. The target rounded the circle at a speed of 6 or 3 times per 1024 points. The mean velocity (MV), mean acceleration (MA), and MA/MV ratio were calculated for the extent of one circle period. And the coefficient of variation (CV) of the shifted distance in each sampling time and the power spectrum by Fast Fourier Transform (FFT) to the acceleration wave were calculated for the total input data. In the free circles, the MV and logarithm of MA varied widely and showed positive correlations. In contrast, those of the pursuit circles converged narrowly near the values of the target. On the other hand, in the SCD group, many patients could not draw the small free circle.(ABSTRACT TRUNCATED AT 250 WORDS)

[Neurophysiological studies of minamata disease with HTLV-I associated myelopathy--a case report].

In both Minamata disease (MD) and HTLV-I associated myelopathy (HAM), sensory disturbance is one of the most characteristic clinical symptoms. We have examined median nerve SSEPs (MN-SEP) and posterior tibial nerve SEPs (PTN-SEP) of both patient groups, and reported their specific abnormalities. MN-SEP of MD patients never showed any conduction delay nor conduction block at the cervical cord. However, they demonstrated the initial positive cortical response with low amplitude instead of the initial negative response (N20) seen in healthy subjects. In PTN-SEP, MD patients showed the initial positive cortical response with significantly shorter latency and lower amplitude than healthy subjects. These findings have never been seen in any other diseases. On the other hand, the conduction delay and conduction block on peripheral nerve, spinal cord and/or intracranial sensory tracts have been demonstrated in many cases with HAM. The patient was a 60-year-old man. About 40 years ago, he suffered with typical clinical symptoms of MD such as cerebellar ataxia, intention tremor and sensory disturbance of upper and lower extremities, and then his condition was complicated with progressive spastic paraplegia and urinary bladder dysfunction since 30 years ago. Both MN-SEP and PTN-SEP were studied so that we could make the electrophysiological differential diagnosis of MD and HAM. His MN-SEP indicated both the conduction delay at his cervical cord and intracranial sensory tract and the initial positive potential from cephalic recording. Furthermore, his PTN-SEP demonstrated severe conduction block at the spinal cord and neither cervical response (N28) nor cortical response (P37) was evoked. In conclusion, the clinical electrophysiologic studies supported our notion that the case might be affected with both MD and HAM.

Quantitative analysis of tremor in Minamata disease.

Applying the techniques of power spectrum and pulse correlation, we carried out a quantitative analysis of tremor in normal subjects, patients with methyl mercury poisoning (Minamata disease) and patients with other diseases. We found that tremor of methyl mercury poisoning was different from physiological tremor and the other pathological tremors in frequency and amplitude.

[Enzyme immunoassay for serum 18-hydroxycorticosterone and its clinical application].

An enzyme immunoassay for serum 18-hydroxycorticosterone was established using alkaline phosphatase as a label. The antiserum for 18-hydroxycorticosterone was produced by immunization of rabbits with 18-hydroxycorticosterone 3-(o-carboxymethyl) oxime conjugated to bovine serum albumin. Sephadex LH-20 column chromatography was used to separate 18-hydroxycorticosterone from other steroids in serum samples. The minimal detectable amount of 18-hydroxycorticosterone was 50 pg/tube, and the measurable range was from 5 to 1000 ng/dl when a 1.0 ml serum sample was used. Intra- and inter-assay coefficients of variance were 5.0% (n = 6), and 5.8% (n = 6), respectively. In normal controls the serum 18-hydroxycorticosterone level was 4.8 approximately 34.0 ng/dl (mean +/- S.D. = 17.1 +/- 9.0 ng/dl) on an unrestricted diet. Seven out of 8 patients with aldosterone-producing adenoma had above-normal serum 18-hydroxycorticosterone levels. Serum 18-hydroxycorticosterone increased and decreased significantly following ACTH and dexamethasone administration, respectively. In essential hypertensive patients, serum 18-hydroxycorticosterone was high during a low-sodium diet and was suppressed remarkably by captopril. These observations support the previous reports that adrenal 18-hydroxycorticosterone synthesis is dependent on both ACTH and the renin-angiotensin system. The present method is sufficiently sensitive and producible, avoids the use of radioisotopes and is quite satisfactory for clinical use.