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ABSTRACT: BACKGROUND: Accumulating evidence indicates an association of Alzheimer's disease (AD) with the metabolic syndrome (MetS), characterized by visceral fat accumulation with insulin resistance and altered secretion of adipocytokines such as adiponectin and leptin. The renin-angiotensin system (RAS) regulates blood pressure and insulin resistance. Recent studies suggest that the RAS plays crucial roles in cognitive functions and that adipocytokines exert neuroprotective activity in the brain. We investigated whether RAS blockers (RASB) affect adipocytokines and cognitive function in patients with AD. METHODS: We studied 78 patients with a diagnosis of probable AD according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition and 106 nondemented control subjects who visited our clinic with a main complaint of headache or dizziness. We examined retrospectively the effects of RASB on adipocytokines and cognitive decline in patients with AD who were divided into three groups: hypertension treated with RASB (HT-RASB; n = 17), hypertension treated with other antihypertensive drugs (HT-other; n = 34), and no hypertension (non-HT; n = 27). RESULTS: The HT-RASB group had a significantly higher serum leptin level and a relatively larger visceral fat area than the other groups, because of the bias toward patients with MetS in this group. The HT-RASB group also had a significantly lower immunoreactive insulin level, a relatively low homeostasis model assessment as an index of insulin resistance, and a relatively high serum adiponectin level among the three groups. Cognitive decline, estimated on the basis of the mean annual decline using the Hasegawa Dementia Scale score was significantly low in the HT-RASB group. CONCLUSION: Treatment with RASB might modulate serum adipocytokines and glucose homeostasis, potentially slowing cognitive decline in patients with AD.
Alzheimer's & dementia: the journal of the Alzheimer's Association 11/2012; · 5.90 Impact Factor
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ABSTRACT: We hypothesized that the unusual and painful abdominal contractions in two of our patients with Parkinson disease (PD) were linked to abdominal muscle hypertrophy. The abdominal pain was aggravated by sitting, standing, or walking, and was characterized by a powerful pulling sensation associated with palpable contractions of the rectus abdominis. When the pain decreased, the camptocormia abated. The thickness of the rectus abdominis and the relative muscle thickness ratio were greater in the two patients with abdominal contractions than in the control patients with PD without abdominal contractions. Palpable painful abdominal contractions could be associated with the presence of hypertrophy of the rectus abdominis visible on CT scan. The abdominal muscle contractions probably contribute to the development a stooped posture.
Journal of Clinical Neuroscience 04/2012; 19(4):624-7. · 1.25 Impact Factor
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ABSTRACT: Abnormalities of both motor and sensory nerve action potentials, similar to those found in demyelinating polyneuropathy, may occur in patients with amyotrophic lateral sclerosis (ALS). We analyzed the clinical features of unusual ALS patients with demyelinating polyneuropathy (DPN) to delineate the characteristics and outcomes of this rare condition. We reviewed three ALS patients with DPN who were confirmed to meet the electrophysiological nerve conduction criteria for DPN among 157 patients with ALS. At the initial neurological examination, one patient had both subjective sensory symptoms and abnormal results of sensory examinations, and one patient had sensory symptoms. Motor weakness of the limbs was present in all patients, and fasciculation was present in two patients. Anti-GalNAc-GD1a IgG antibodies were evident in one. Sural nerve biopsy showed a moderate, marginal reduction in myelin thickness, and teased fiber analysis revealed segmental demyelination and remyelination, but axonal degeneration was found in one patient. The mean interval from disease onset to respiratory failure or death in our three patients and seven previously documented ALS patients with DPN was 43.1 ± 18.7 months. Our findings suggest that survival in ALS with DPN is similar to that in classic ALS.
Amyotrophic Lateral Sclerosis 01/2012; 13(1):125-31. · 3.40 Impact Factor
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ABSTRACT: The middle cerebellar peduncle (MCP) is supplied mainly by the anterior inferior cerebellar artery and partly by the superior cerebellar artery. The bilateral MCP infarctions in previous patients were attributed to alternations of two vessels, such as the unilateral vertebral artery and basilar artery or both vertebral arteries.
We describe a case of bilateral acute infarction of the MCP and the stroke was apparently caused by occlusion of only one vertebral artery.
A 63-year-old man presented with vertigo and auditory distortion, accompanied by difficulty in speaking and walking. Neurological examinations revealed bilateral horizontal nystagmus, scanning speech, and ataxia of the trunk and all four limbs. Brain MRI showed high signal intensity in the both MCPs on diffusion-weighted and T2-weighted images. Enhanced computed tomographic angiography showed fusiform dilatation at the V4 level of the right vertebral artery; a false lumen was evident in the dilatation. Right vertebral angiography showed occlusion from the C1 level to the foramen magnum. Left vertebral angiography revealed a hypoplastic vertebral artery with a maximum diameter of 2.5 mm.
Alternations of the vertebral artery should be considered as a possible cause of MCP infarction, particularly when such anomalies are suggested.
Journal of neuroimaging: official journal of the American Society of Neuroimaging 04/2011; 21(2):e171-2. · 1.72 Impact Factor
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Takao Kiriyama,
Hiroshi Kataoka,
Toshiaki Taoka,
Yasuyo Tonomura,
Mari Terashima,
Masami Morikawa,
Emi Tanizawa, Makoto Kawahara,
Yoshiko Furiya,
Kazuma Sugie,
Kimihiko Kichikawa,
Satoshi Ueno
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ABSTRACT: Features of tumefactive demyelinating lesion (TDL) on magnetic resonance imaging (MRI) can facilitate the differential diagnosis of TDL and neoplastic lesions, but vary considerably among patients. The larger TDL grows, the more difficult it becomes to differentiate TDL from neoplastic lesions. The purpose of this study was to elucidate typical MRI features in 12 patients with large TDL (>30 mm in diameter).
We identified 12 patients with large TDL (six men, six women; age range 17-64 years, median age 27 years) and studied the clinical histories and the results of laboratory and various radiological studies in these patients. All cases of clinically definite multiple sclerosis were diagnosed in accordance with McDonald's revised criteria.
Common MRI features of large TDLs included variable degrees of mass effect (71%) and edema (100%), a T2 hypointense rim (79%), venular enhancement (57%), and peripheral restriction on diffusion-weighted images (50%). Ring enhancement (38%), open-ring enhancement (31%), or decreased N-acetylaspartate ratios on magnetic resonance spectroscopy (22%) were less frequently observed. Brain angiography demonstrated venous dilatations on and around the TDL.
The diagnosis of large TDL is challenging. Our findings suggest that multiple venous dilatations on and around TDLs on angiography can facilitate diagnosis.
Journal of neuroimaging: official journal of the American Society of Neuroimaging 04/2011; 21(2):e69-77. · 1.72 Impact Factor
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ABSTRACT: Brainstem encephalitis is not a classic paraneoplastic syndrome and usually involves monophasic neurological deterioration and has negative magnetic resonance imaging (MRI) findings. We describe a patient with brainstem encephalitis who had elevated anti-Ri antibody levels and double-step neurological deterioration associated with different abnormal lesions on MRI. Immunosuppression with steroids and intravenous immune globulin combined with aggressive treatment of the tumor successfully led to the resolution of brainstem symptoms and MRI lesions. In patients with unusual signs and symptoms of paraneoplastic encephalitis mimicking multiple sclerosis, onconeural antibody studies are recommended.
Journal of Neuro-Oncology 02/2010; 100(1):141-3. · 3.21 Impact Factor
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ABSTRACT: Histopathologically, herpes simplex virus type 1 causes hemorrhagic necrosis. Overt hemorrhage is infrequent in herpes simplex virus encephalitis but can lead to poor outcomes. This report describes a successfully treated case of herpes simplex virus encephalitis associated with subarachnoid bleeding in which real-time polymerase chain reaction was useful for diagnosis.
A 30-year-old previously healthy Japanese woman who had fever and headache for five days presented with disorganised speech, unusual behavior and delusional thinking. Real-time polymerase chain reaction amplification of herpes simplex virus type 1 in cerebrospinal fluid was positive (38,000 copies/mL) and antivirus treatment was started. During the course of her illness, the level of her consciousness decreased in association with desaturation and tachycardia. Thrombosis of the right pulmonary artery trunk with pulmonary embolism was evident on enhanced chest computed tomography. In addition, cranial computed tomography revealed subarachnoid and intraventricular bleeding. Intravenous heparin (12,000 U/day) was started and the dose was adjusted according to the activated partial thromboplastin time for about a month (maximum dose of heparin, 20,400 U/day). After the treatments, her Glasgow coma score increased and the thrombosis of the pulmonary artery trunk had disappeared.
The present case raises the question of whether anticoagulant treatment is safe in patients with herpes simplex virus encephalitis complicated by subarachnoid bleeding.
Journal of Medical Case Reports 01/2010; 4:310.
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ABSTRACT: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) alleviates motor disability of patients with Parkinson's disease (PD). Mental changes and other adverse events are common, but typically transient. Severe complications such as intracerebral haemorrhage or infection are rare, but 6 of 73 patients who underwent STN-DBS died of pneumonia, cardiac failure or pulmonary embolism. We describe a patient with PD who had sudden respiratory difficulty due to a fixed epiglottis after STN-DBS. This symptom was confirmed to be related to STN stimulation on fibre-optic examination of the larynx.
Case Reports 01/2009; 2009.
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International journal of hematology 09/2008; 88(3):345-7. · 1.17 Impact Factor
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ABSTRACT: We describe a successful outcome of long-term interferon beta-1b therapy in a patient who had multiple sclerosis (MS) with positive serum autoantibody to muscle acetylcholine receptor (AChR-Ab). Because of the reported possible causative linkage between interferon beta-1b and myasthenia gravis (MG), the presence of the pathogenic antibody complicated therapeutic strategies. We carefully observed the patient for further 6 months before the treatment, excluding symptomatic MG. The interferon beta-1b therapy then provided a clinical benefit. Hopefully this report will allow MS patients in similar situations to make more rapid, unprejudiced judgments than our patients.
Clinical Neurology and Neurosurgery 05/2007; 109(3):277-8. · 1.58 Impact Factor
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Movement Disorders 03/2007; 22(3):437-9. · 4.51 Impact Factor
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Internal Medicine 07/2005; 44(6):679-81. · 0.94 Impact Factor
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Neurology 02/2005; 64(2):389. · 8.31 Impact Factor
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ABSTRACT: Early-onset ataxia with ocular motor apraxia and hypoalbuminemia (EAOH) is one of the most common forms of autosomal recessive cerebellar ataxia. We identified six new alternative transcripts produced by the aprataxin gene responsible for EAOH. Total eight transcripts encoded truncated proteins that were located within the nucleus or cytoplasm and showed different binding abilities to wild-type (WT) aprataxin. Thus, the alternative splicing increases the molecular diversity of aprataxin and the expression profiles of these transcripts in various tissues may be related to the tissue-specific phenotypes.
Neuroscience Letters 09/2004; 366(2):120-5. · 2.11 Impact Factor
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ABSTRACT: Humanin (HN) and S14G HN (HNG) are recently discovered polypeptides that rescue cells from death induced by multiple different types of familial Alzheimer's disease genes and by amyloid-beta. However, the cytoprotective activity of these peptides against other cell death-inducing stimuli remains unclear. In this study, we demonstrated, using three different methods (MTS assay, caspase-3 assay, and detection of DNA fragmentation), that both HN and HNG protect PC12 cells from death elicited by serum deprivation. This implies the potential of the peptides to rescue cells from a broad spectrum, if not all, of cell death-inducing factors. Further investigations on HN may lead the possible application of this peptide as therapeutic agent for the treatment of other neurodegenerative diseases.
Neuroreport 06/2002; 13(6):903-7. · 1.66 Impact Factor
