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We report the case of a 40-year-old woman, with endometriosis, who presented with a history of foot drop and cyclic sensory disturbance of the right lower limb. She was initially diagnosed with lumbar disc herniation. Neurological examination revealed muscle weakness and sensory disturbance associated with the right sciatic nerve. Nerve conduction studies revealed a low amplitude sensory nerve action potential in the right superficial fibular and sural nerves. Pelvic magnetic resonance imaging revealed an endometriotic cyst in the right ovary, and an endometriotic lesion extending from the right ovary, pelvis, and the right sciatic nerve. Though her symptoms moderately improved with hormonal therapy, the foot drop remained. Our case and previous reports suggest that endometriosis with sciatic neuropathy shows cyclic neurological symptoms during menstruation, with a higher incidence on the right extremity. This case highlights that endometriosis should be considered as a potential differential diagnosis in women of reproductive age with sciatic nerve dysfunction. Its cyclic neurological manifestations should be investigated.

A 63-year-old woman was diagnosed with Guillain-Barré syndrome (GBS), and intravenous immunoglobulin (IVIg) therapy was initiated. On the second day of IVIg therapy, she became less alert (JCS III-200) and had hyponatremia. Brain MRI showed vasogenic edema in bilateral occipital lobes, which disappeared afterwards. Her clinical course and MRI findings were consistent with those of posterior reversible encephalopathy syndrome (PRES). As a result of considering the timing of the onset of GBS and PRES and the degree of hyponatremia and hypertension in some documented patients, the cause of PRES onset in this case is considered to be IVIg therapy itself and IVIg therapy-induced hyponatremia.

We report a case of meningeal carcinomatosis that needed to be distinguished from subarachnoid hemorrhage. A 67-year-old female with acute severe headache was admitted to a previous hospital. Since high intensity signal was detected within the parietal cerebral sulci on the right side on brain FLAIR MRI, cerebral angiography was performed due to suspicion of subarachnoid hemorrhage. However, no vascular abnormality was observed. Then, cerebral spinal fluid was collected, which showed an increase in cell count, suggesting meningitis. She was transferred to our hospital for evaluation of neurological disease. After admission to our hospital, there was an episode of hematemesis. Upper gastrointestinal endoscopy was performed, and advanced gastric cancer was found. She was diagnosed as having meningeal carcinomatosis due to gastric cancer. Meningeal carcinomatosis should be considered in addition to subarachnoid hemorrhage when a patient with acute headache shows high intensity signal within the cerebral sulci on brain FLAIR MRI.

To investigate whether the striatal dopamine receptor function is involved in the development of vascular parkinsonism (VP), a positron emission tomography (PET) study was conducted on 9 patients with VP by using [11C] N-methylspiperone as the tracer. The rate of binding availability in the striatal dopamine D2 receptor (k3) was determined semiquantitatively, and the values were compared to the predicted normal values based on the results from 7 normal volunteers. Of 9 patients with VP, the normalized D2 receptor binding [%k3] was more than 90% in 5 patients, 89 to 87% in 3, and 75% in one. These values showed no evident correlation with the Hoehn and Yahr stage. The laterality of the striatal %k3 did not correspond to that of the parkinsonism. Thus, the striatal dopamine D2 receptor binding was not severely impaired and did not correlate with the neurological status in patients with VP. This may indicate that striatal dopamine D2 receptor function is not primarily associated with the development of the parkinsonism in VP.

We reported a 74-year-old male case of progressive supranuclear palsy (PSP) who responded to tandospirone citrate, a serotonin receptor (5-HT1A) agonist. The patient manifested postural instability and gait disturbance at 71 years. Additionally, he showed vertical gaze paresis, regidity of the neck, extremities and trunk, bradykinesia and mild cognitive impairment. A brain MRI revealed moderate atrophy of bilateral frontal/temporal lobes and of midbrain tegmentum one year after the onset. The patient had been diagnosed as PSP and treated with L-DOPA. However, L-DOPA therapy showed only transient response for a few months. His symptoms deteriorated gradually, and he became unable to sit, stand up or walk by himself. Tandospirone citrate was additionally administered at 30 mg/day. Rigidity and bradykinesia were remarkably improved in two weeks after the start of tandospirone treatment. He became able to stand up and walk a short distance with supports in four weeks. Cognitive disturbance was also slightly improved. Tandospirone citrate was effective on our case of PSP, especially on rigidity. Our findings suggest that combination of levodopa and tandospirone citrate is a useful therapy for PSP.

We report a case of aortic coarctation who showed a Brown-Séquard syndrome due to the aneurysm of the anterior radicular artery. A 71-year-old right-handed hypertensive woman was admitted to the Research Institute for Brain and Blood Vessels because of subarachnoid hemorrhage in 1984. No aneurysm was detected even on the four-vessel cerebral angiography. However, the left subclavian artery was occluded associated with the coarctation. In 1997, she complained of numbness of the right lower extremity, which gradually expanded to the back and the right upper extremity. On neurological examination, she exhibited a mild weakness of the right lower extremity and a dissociated sensory disturbance below the level of C5. The cervical MRI showed a space occupying lesion at the level of C4. The right vertebral angiography revealed an aneurysm of the left anterior radicular artery at the level of C4, which compressed the spinal cord. Previously only a few cases of an aortic coarctation associated with the radicular artery aneurysm were reported in our country. The age of onset of this case was older than in the previous cases, and the location of the aneurysm was higher than those of the previous cases. Probably due to the occlusion of the left subclavian artery, the transverse collateral circulation was produced from the right to the left anterior radicular arteries at the level between C2 and C5, causing a radicular artery aneurysm in this patient.

Long-term follow-up study with positron emission tomography (PET) has been conducted in a patient with superficial siderosis for ten years. A 63-year-old right-handed woman began to exhibit a cerebellar ataxia when she was 52 years old. Thereafter she has been exhibiting a slowly progressive course of pyramidal signs, hearing loss, anosmia, bilateral sciatica and memory disturbance in addition to the cerebellar ataxia. Series of x-ray CT and MRI disclosed a progressive atrophy of the cerebellum, specifically in the superior vermis, and a mild diffuse atrophy in the cerebral hemispheres, whereas no significant atrophy was seen in the brainstem. A marked hypointensity was seen along the rim of the brain structures including brainstem, cerebellum, sylvian fissures and the medial temporal lobes on MR T 2-weighted images. This hypointensity was also found at the edges of the third and fourth ventricles. These findings were regarded as haemosiderin deposit. By using oxygen-15, PET was carried out repeatedly with ten-year interval. In the initial PET study, both cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were mildly decreased in the cerebellar hemispheres and the occipital cortices. The follow-up PET study revealed a progressive reduction of CMRO2 in the brainstem, cerebellar hemispheres and temporal cortices including the hippocampus in which the haemosiderin deposition was marked on MRI, whereas the reduction of CBF was not advanced as compared with CMRO2. It was suggested that the progressive reduction of CMRO2 in the brain sites where the haemosiderin deposition was observed on MRI reflected the clinical course of neurological deterioration.

To elucidate the pathophysiology underlying the dementia due to chronic intoxication of toluene, a positron emission tomography was carried out in a 24-year-old right-handed man who had been sniffing thinner which contains toluene for 6 years. In addition to the cerebellar ataxia and pyramidal signs, this patient exhibited a mental deterioration including recent memory disturbance: verbal IQ was 52, performance IQ was 52 and total score was 51 on WAIS-R. MRI revealed a mild diffuse cortical atrophy, symmetrical hyperintensity lesions in the corticospinal tracts including corona radiata posterior limb of the internal capsule and ventral part of the pons, and hypointensity lesions in the both thalami on T2-weighted images, whereas the changes in the deep white matter was relatively mild on T2-weighted images. In PET, both cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were diffusely decreased bilaterally, and specifically in both hippocampi, they were reduced as low as 61% of the normal values as obtained from 12 young normal volunteers. Additionally, in the frontal cortex, CBF and CMRO2 were 60% and 71% of the normal values, respectively. Although the dementia due to chronic toluene intoxication has been assumed to be closely related to the degree of the cerebral white matter lesions based on the MR findings, the present results suggest that the mental deterioration including recent memory disturbance seen in the early stage of chronic toluene intoxication is associated with the hypoperfusion and hypometabolism in the hippocampus and frontal limbic system.