Rhabdomyolysis lesions showing magnetic resonance contrast enhancement.

Although T2-weighted magnetic resonance imaging (MRI) was reported to be useful for depicting rhabdomyolysis lesions, little is known as to the usefulness of gadolinium-enhanced T1-weighted imaging. The authors performed noncontrast and postcontrast T1-weighted MRI along with T2-weighted MRI in a patient with rhabdomyolysis in the chronic phase. Non-contrast T1-weighted imaging revealed no abnormality, whereas postcontrast T1-weighted imaging demonstrated lesions more definitively than T2-weighted imaging. Gadolinium-enhancement study may contribute to the MRI diagnosis of rhabdomyolysis.

Presymptomatic brain lesions on MRI in a patient with intravascular malignant lymphomatosis.

A 58-year-old man with a intravascular malignant lymphomatosis initially developed myeloradiculopathy without cerebral symptoms. His MRI, however, demonstrated solid, wedge-shaped, and well-demarcated lesions in the deep white matter and a string-shaped lesion along with nerve fibers in the splenium of corpus callosum. A variety of cerebral symptoms manifested a month afterward. The possibility of this disease should be considered in cases of undiagnosed myeloradiculopathy with such silent brain lesions.

Halothane-induced cytotoxicity in isolated rat hepatocytes: an electron microscopic study.

To determine the direct cytotoxicity of halothane for liver cells, the effects of this agent on isolated rat hepatocytes were investigated by electron microscopy and by examining cell viability. Soon after treatment with lower concentrations of halothane (0.5% and 0.75%), there were marked changes in the plasma membrane. Cell viability was reduced to 70% of the control. At higher concentrations of halothane (1% and 3%), degeneration of mitochondria was noted. Cell viability was reduced to 40% of the control. Halothane, at lower concentrations, appeared to induce early morphological alterations of the plasma membrane, while higher concentrations damaged the organella.

[A case of multiple cerebral arterial thrombosis due to congenital protein C deficiency].

We report a 49-year-old man who had right hemiparesis and motor aphasia. A computed tomography revealed hypodense areas in the left frontal subcortex. A cerebral angiography demonstrated occlusion of the left distal internal carotid artery and both anterior cerebral arteries, as well as stenosis of the left internal carotid artery at the cervical portion. The second angiogram obtained a month later showed no changes. The diagnosis of atherothrombotic cerebral infarction was established on the basis of clinical profile and angiographic findings. Protein C activity and antigen levels were reduced to approximately one half of the normal level in the patient and his brother. The patient had no other risk factors for stroke. Protein C deficiency has been considered one of the risk factors for thrombotic diseases. Venous thrombosis is the most common clinical manifestation, whereas arterial thrombosis is relatively rare. It is generally believed that arterial ischemic stroke associated with protein C deficiency occurs with embolic mechanism, and atherothrombotic infarction is extremely rare. This is the first report suggesting the possibility that protein C deficiency can cause cerebral thrombosis.

[A case of progressive continuous muscular rigidity and painless and rhythmic muscle spasm associated with autoantibody against glutamic acid decarboxylase].

We described a 60-year-old man with 5-year history of insulin dependent diabetes mellitus who developed continuous rigidity of truncal muscle and painless, rhythmic muscular spasm of trunk and proximal lower and upper extremities. The rigidity continued even in sleep. The painless muscle spasm was often precipitated by volitional movement and emotional stimuli. Intravenous administration of diazepam strongly attenuated the muscle spasm as well as truncal rigidity. Surface electromyography showed the continuous contraction of abdominal and paraspinal muscles. The rhythmic, clonic spasm of shoulder, triceps brachii, intercostal, abdominal, paraspinal and quadriceps femoris muscle induced by voluntary neck flexion was not compatible with typical stiff-man syndrome. Antibody against glutamic acid decarboxylase (GAD) was detected in the serum and cerebrospinal fluid of this patient. His condition was getting well with oral intake of sodium valproate. While painless, rhythmic spasm and persistent rigidity during sleep ruled out the patient from typical stiff-man syndrome, he was supposed to have the same pathophysiological mechanism as the anti-GAD autoantibody positive stiff-man syndrome.

The influence of upper respiratory tract surgery on respiratory function evaluated by oxygen saturation.

To evaluate the influence of upper respiratory tract surgery on respiratory function, we used a pulse oximeter to measure the arterial oxygen saturation in 40 patients (ASA 1 or 2) during surgery under local anesthesia. The patients were divided into four groups: a control group of 10 patients who underwent surgery not involving the upper respiratory tract, and three upper respiratory tract surgery groups of 10 patients each underwent surgery on the nasal cavity alone (group 1), on the oral cavity alone (group 2), and on both the oral and nasal cavities (group 3). Groups 1 and 2 showed little desaturation compared to their baseline levels and the control group, while group 3 showed a mild desaturation even at the beginning of surgery and this gradually turned to a moderate or severe desaturation. This was due to both the extension of the surgical zone to the nasal and oral cavities and to ventilatory distress produced by massive bleeding and aspiration of secretions. Thus, the pulse oximeter is a useful monitor for upper respiratory tract surgery involving both general and local anesthesia. It allows the identification of hypoxia so that remedial therapy can be instituted.

Leakage of mitochondrial and cytosolic GOT in isolated rat hepatocytes exposed to halothane: an immunohistochemical study.

The leakage of mitochondrial (m-) and cytosolic (s-) aspartate aminotransferases (glutamic-oxaloacetic transaminase: GOT) from isolated hepatocytes exposed to halothane was investigated immunohistochemically. In control isolated hepatocytes, a large number of cells were immunopositive (m-GOT, 85%; s-GOT, 98.5%) at various intensities. Reaction products of m-GOT-immunohistochemistry (m-GOT-I) were seen exclusively in mitochondria, while those of s-GOT (s-GOT-I) were seen in the cytoplasm. When treated with low concentrations of halothane (up to 0.75%), the number of strongly m-GOT-I-immunopositive cells was reduced to half, while that of s-GOT-I showed no noticeable change. The number of m-GOT-I-immunonegative cells showed a negligible increase, while that of s-GOT-I increased gradually. At higher concentrations of halothane (1% or more), strongly immunopositive cells in both m- and s-GOT-I almost disappeared, while immunonegative cell numbers predominantly increased. This study showed that the isolated hepatocyte system was not homogeneous with regard to the quantity of GOT isozymes, and that halothane could induce the leakage of these isozymes from hepatocytes, along with inducing ultrastructural abnormalities, even at the lowest concentration used (0.5%). Furthermore, the data appear to indicate that the sensitivity of isolated hepatocytes to halothane is dependent on the nature of the hepatocyte itself and on the nature of both types of GOT isozymes.

Effect of chronic middle cerebral artery stenosis on the local cerebral hemodynamics.

In 36 patients with angiographically proven middle cerebral artery (MCA) stenosis, local cerebral hemodynamics were studied employing angiography, 133Xe inhalation regional cerebral blood flow (rCBF) measurements and CT scans. They had transient ischemic attacks in 8 and completed stroke in 28. The patients with less than 50% stenosis (n = 16) had no hemodynamic abnormality in angiographical and rCBF examinations. The infarction in this group was small and located in the basal ganglia area. The patients with 50 to 74% stenosis (n = 9) often revealed a delayed filling of MCA branches in the angiography, however, they showed no significant rCBF reduction. The infarction in this group was also small and located in the basal ganglia area. The patients with 75 to 99% stenosis (n = 11) exhibited a significant flow depression both in angiographical and rCBF examinations. Three of them had large cerebral infarction in the watershed zone or the cerebral cortex. The results of the present study suggest that the hemodynamic effect of MCA stenosis begins to manifest at 50% in grade and becomes apparent at 75%. The danger of hemodynamic crisis as well as the risk of large cerebral infarction may increase when MCA stenosis exceeds 75% in grade.