The relationship between the features of MRI in brainstem and pathological findings was investigated in eight autopsy cases with progressive supranuclear palsy (PSP). Features of T1-weighted images at midbrain level were atrophy of tegmentum and tectum, and dilatation of aqueduct. Histologically, these findings were consistent with atrophy of periaqueductal gray matter, quadrigeminal plate, and tegmentum. In these lesions, we detected neuronal loss, decrease in density of myelinated fibers, gliosis, rarefaction of tissues, and tau-positive structures such as neurofibrillary tangles (NFTs), glial fibrillary tangles (GFTs) and neuropil threads. At pons level, atrophy of tegmentum, atrophy of pontine base, and dilatation of prepontine cistern were found. Tau-positive structures were observed not only in tegmentum but also in pontine base. The density of the tau-positive structure was closely related to the severity of atrophy. Features of T2-weighted images were high intensity in the periaqueductal lesion and tegmentum in pons. In these lesions, severe histological findings were detected. The MRI features in brainstem were closely related to the histological findings as PSP.

CT and MRI have become indispensable methods for the diagnosis of stroke or the investigation for the disease. The use of these auxiliary diagnostic procedures, especially of MRI, has made possible the accurate diagnosis of lesions of the posterior cranial fossa. The flow void in MRI has made it feasible to infer severe stenosis or occlusion of the main arteries before undertaking angiography. The silent stroke or white matter abnormalities in the vicinity of the lateral ventricle observed in CT or MRI have become a serious clinical problem and these are generally considered risk factors for stroke. Obviously, CT and MRI have proven effective in this area, yet their findings do not always make it readily possible to infer the nature of cerebral arteries involved. Recently, here have been attempts to classify infarcts in the region of perforating branches of the middle cerebral artery. With the diversification of therapeutic approaches for stroke in the days to come, the effort to encourage such insight on the basis of non-invasive testing will be increasingly important.

A 55-year-old man first noted a swelling on his back in September 1990, when CT scan of his chest suggested a pleural fistula and a cold abscess. In the following month, he became pyrexial and felt nauseated with headache. Subsequently he was transferred to our hospital. Results of neurological examination were abnormal only in that he had neck stiffness and bilateral nystagmus with drowsiness. Cerebrospinal fluid (CSF) showed turbid yellowish fluid with an opening pressure of 360 mmH2O, a protein content of 173 mg/dl, a glucose level of 19 mg/dl, and a white blood cell count of 3,024/ml (75% polymorphs, 25% lymphocytes). Tryptophane test was positive. No bacteria, fungi or acid-fast bacilli were seen on direct smear. Adenosine deaminase activity in CSF was 13.9 IU/l. Antibiotics, antituberculous drugs, corticosteroids and glycerol were administered. The clinical course in the hospital was satisfactory for the next two months, but a contrast enhanced CT scan showed prominent enhancement in the left choroid plexus, and MRI revealed another mass in the subarachnoidal space under the right frontal lobe. An open biopsy was done on the massive lesion in the frontal lobe. Macroscopically, this lesion was an encapsulated granulomatous one. On the other hand, there were groups of epitheloid cells with micronecrosis in their centers microscopically. These findings were compatible with tuberculoma, in spite of the absence of acid-fast bacilli or caseous necrosis. Medication was intensively continued: a follow-up CT showed gradual reduction of the choroid plexus lesion and shrinkage of the left lateral ventricle.

Nineteen patients (15 men, 4 women) with occlusion of the vertebrobasilar artery were studied in order to identify possible pathomechanism and to define the site of arterial occlusion and the topography of ischemic lesion of the cerebellum. Their mean age at onset was 66.7 years and the final clinicopathological diagnosis were thrombosis of the basilar artery (BA) in 15 patients and embolism in 4. The occlusion of the BA was contiguous to that of the vertebral artery in ten patients. Of these, the occlusion was localized to the caudal portion of the BA in two, to the middle portion in six, and extended to the rostral portion in two. In eight patients, the arterial occlusion was restricted to the BA. Occlusions of the middle portion were observed in four and that of rostral portion in two; in the other two patients, the whole BA was occluded. In one patient, there was no occlusion in the vertebro-basilar artery at the postmortem examination, but infarctions of the base of pons, bilateral cerebellar hemispheres and occipital lobes were confirmed, suggesting recanalization of the occluded BA. Cerebellar lesions were observed in all nineteen patients. Involvements of the area supplied by the superior cerebellar artery (SCA) were found in seventeen, while that of the posterior inferior cerebellar artery (PICA) only in ten. Eight patients had cerebellar lesions supplied by both SCA and PICA. These facts suggest that cerebellar lesions are rather frequent and the SCA areas are more involved than those of the PICA in fatal patients with occlusion of the BA.(ABSTRACT TRUNCATED AT 250 WORDS)

A case of a 29-year-old woman with idiopathic hypoparathyroidism was reported. There were neither endocrine nor neurological disorders among her family, except for her mother's hearing loss. She had been suffering from insulin-dependent diabetes mellitus since 21 years of age, and was noticed to be hard of hearing for several years, but never been examined. At the age of 27, choreic movement on her left upper limb and gait disturbance appeared. A year before admission, gait disturbance gradually developed and she could not walk any more. On admission, her height was 137.2 cm and her weight 36.5 kg. She had a round face, uneven teeth and borderline metacarpal sign on her right hand. On neurological examination, Parkinsonism, bucco-lingo-masticatory dyskinesia and bilateral extensor planter reflex were present, but tetany was not observed anywhere. Serum calcium was 3.9 mEq/l, and serum phosphorus 5.3 mEq/l. A CT scan of brain revealed calcifications in the bilateral basal ganglia and thalami, low density area in the left putamen, and atrophy of both caudate nuclei. Serum PTH was less than 100 pg/ml. Ellsworth-Howard's test showed hyperresponsiveness in the secretion of urinary phosphorus and cyclic-AMP. Other endocrinological studies showed no abnormality except for hyporesponsiveness in the secretion of insulin on glucose tolerance test. On the basis of these results, a diagnosis of idiopathic hypoparathyroidism with insulin-dependent diabetes mellitus was made. Administration of alfacalcidol returned serum calcium and phosphorus to normal with considerable clinical benefit. Parkinsonism was gradually improved and she became to be able to walk with a cane after one year of treatment. But buco-lingo-masticatory dyskinesia were not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)