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Biomedical subjects

Kunio Shimazu

Publications and source records attributed to Kunio Shimazu.

At least 19 recordsLinked to original sources
PubMed2006

Parkinsonism in type I Gaucher's disease.

The majority of patients with type I Gaucher's disease never develop neurological signs or symptoms. However, several case reports of Parkinson's disease associated with type I Gaucher's disease have been published, suggesting a genetic link between the two diseases. Hence, detailed clinical investigations are required when the two diseases occur simultaneously, in order to determine whether this is coincidental or whether a true association is present. We present a Japanese man in whom parkinsonism was associated with type I Gaucher's disease. Findings of brain positron tomography (PET) and metaiodobenzylguanidine (MIBG) cardiac scintigraphy are presented.

3-Iodobenzylguanidine↗
PubMed2006

Effect of L-DOPA on nitric oxide production in striatum of freely mobile mice.

In Parkinson's disease, nitric oxide (NO) and other free radicals are thought to be involved in neuronal degeneration. Furthermore, L-DOPA is suggested to have a cytotoxic action on dopaminergic neurons. We studied 24-h NO production and the effect of L-DOPA on this in freely mobile mice using in vivo microdialysis. A microdialysis probe was implanted into the right striatum 12 h before the experiment. This dialysis probe was perfused with Ringer solution for 100 min, then with 20, 50, or 100 nM L-DOPA for 20 min, and finally with Ringer solution. Dialysate fractions were collected every 20 min for 4 h. Production of nitrite and total NO were significantly higher during daytime than during nighttime. Nitrate production was increased significantly by L-DOPA. NO production in the striatum appears to exhibit a diurnal rhythm and to increase with exposure to L-DOPA.

Analysis of Variance↗
PubMed2006

[A case of isolated hypoglossal nerve palsy probably due to dural arteriovenous fistula].

We report here a case of isolated hypoglossal nerve palsy probably caused by dural arteriovenous fistula (DAVF). A 51-year-old woman was admitted to our hospital complaining headache, tinnitus, and tongue atrophy. Three years before, she first experienced right-sided pulsatile headache and tinnitus which persisted until admission. One week before, she noticed her tongue deviated to right. On admission, physical and neurological examinations showed no abnormal findings except for bruits on right neck and bilateral orbital areas, and atrophy of right tongue. Brain MRI was not remarkable. MRA and conventional angiography disclosed DAVF. We conclude that differential diagnoses for isolated hypoglossal paralysis should include DAVF.

Central Nervous System Vascular Malformations↗
PubMed2006

[A case of acute idiopathic autonomic neuropathy improved by intravenous immunoglobulin].

We describe a case of acute idiopathic autonomic neuropathy (AIAN) in which intravenous administration of immunoglobulin (IVIg) proved effective. A 32-year-old man was admitted with orthostatic dizziness. Fever and headache first developed 24 days earlier, and persisted for 10 days, when orthostatic dizziness developed and prevented him from walking. Hypohidrosis, constipation and impotence also developed. Neurological examinations revealed no abnormalities. Cerebrospinal fluid obtained showed pleocytosis (26/microl) and an increased level of protein (70mg/dl). A head-up tilt test revealed that blood pressure decreased from 120/60mmHg when supine to 60/ 40 mmHg in a head-up position, and the patient complained of dizziness. Plasma noradrenaline concentration was 26pg/ml when supine and 44pg/ml in a head-up position. Results of MIBG cardiac scintigraphy were normal. Dizziness disappeared after initiating IVIg (0.4 g/kg/day). A head-up tilt test was performed 7 days after IVIg, revealing blood pressures of 106/61mmHg when supine and 103/71mmHg in a head-up position. These results suggest that IVIg should be considered as a choice to treat early AIAN.

Acute Disease↗
PubMed2006

[Sweetness dysgeusia in a case of SIADH caused by lung carcinoma].

A 56-year-old woman, with dysgeusia in which nearly all food was felt as sweet, was admitted to our hospital seeking for treatment. Serum sodium concentration was 113 mmol/L, but serum creatinine, zinc, urea nitrogen, and potassium, as well as blood glucose, were all within normal ranges. Dysgeusia disappeared when serum sodium level was normalized, but recurred when hyponatremia relapsed. She was diagnosed as having large cell lung carcinoma. We considered that the cause of hyponatremia was inappropriate secretion of antidiuretic hormone (SIADH) due to lung carcinoma. Miraculin is one of taste-modifying substances which fits the sweet receptor site and induces a strong sweet taste. We considered that taste-modifying substances same as miraclin are involved in the pathophysiology of this disease.

Carcinoma, Large Cell↗
PubMed2006

[Reversible posterior leukoencephalopathy syndrome in Hashimoto's encephalopathy: a case report].

A 45-year-old woman with breast cancer was admitted to our hospital because of several episodes of disturbed consciousness and generalized convulsions. While these symptoms resolved quickly, dysphagia and bilateral blepharoptosis persisted. Neurological findings were improved by steroid therapy. MRI on the first hospital day showed T2/FLAIR high intensity lesions in both occipital lobes, but these lesions diminished on the 8th day, indicating reversible posterior leukoencephalopathy syndrome. A new lesion appeared in the left temporal lobe on the 8th day. A diagnosis of Hashimoto's encephalopathy (HE) was made due to the following features: 1) encephalitis not due to herpes simplex virus, 2) high titers of antithyroid antibodies in serum, 3) marked effectiveness of steroid therapy, and 4) antibodies against the amino terminal of alpha-enolase, a specific antigen for HE.

Autoimmunity↗
PubMed2005

QSART in idiopathic pure sudomotor failure.

QSART (quantitative sudomotor axon reflex testing) was performed in a patient with idiopathic pure sudomotor failure. Generalized reduction in thermoregulatory sweating and complete absence of axon reflex sweating were observed, suggesting a deficit of sweat gland cholinergic synaptic transmission or receptors. QSART responded promptly to treatment. Putative pathophysiological mechanisms are discussed.

Adolescent↗
PubMed2005

[Aging of the autonomic nervous system].

Aging is associated with structural and functional changes in the autonomic nervous system (ANS), which innervates the whole body, and its altered function may influence almost all body systems. Changes related to aging are found in autonomic nerves and ganglia, and ANS controlled functions including cardiovascular functions. Much of the current knowledge about age-related changes in sympathetic nervous function is derived from studies of circulating catecholamine levels, norepinephrine kinetics and microneurographic recordings from sympathetic nerves of skeletal muscle. Significant evidence suggests that basal plasma noradrenaline levels increase with age. These data indicates that healthy aging is associated with elevated basal sympathetic nervous activity. In contrast, the reactivity of the sympathetic and the parasympathetic nervous activity are reduced with aging.

Aged↗
PubMed2004

[Diplopia in Wallenberg's syndrome].

The incidence and mechanism of diplopia were investigated in 31 patients with Wallenberg's syndrome resulting from acute dorsolateral medullary infarction. Diplopia was found in 10 of 31 patients (32%), with 5 patients reporting vertical diplopia alone and 5 reporting vertical and horizontal diplopia. Diplopia in Wallenberg's syndrome is considered to be caused by a lesion involving the otolith-ocular system. Vertical diplopia is simply explained by ocular skew deviation due to a lesion involving the vestibular nucleus; in which the affected eye becomes deviated inferiorly. In this situation, rotation of the eye due to ocular tilt reaction also occurs. Concomitant horizontal diplopia may require involvement of the medial longitudinal fasciculus (MLF), which produces skew deviation in mirror image; the unaffected eye becomes deviated inferiorly. When downward deviation of the eye affected by dysfunction of the vestibular nucleus and that due to MLF dysfunction affecting the other eye are comparable, only horizontal diplopia becomes apparent. MLF syndrome may be accompanied by paralytic pontine exotropia (PPE) or non-paralytic pontine exotropia (NPPE), both of which may also participate in the appearance of horizontal diplopia.

Adult↗
PubMed2004

[Central post-stroke pain in Wallenberg syndrome].

We analyzed clinical characteristics of central post-stroke pain (CPSP), constant and burning pain, in 32 patients with Wallenberg syndrome due to infarction. CPSP developed in 44% (14/32) of the patients; 8 in acute stage (within 4 days after the stroke) and 8 in chronic stage(10-120 days after the stroke). Apart from one exceptional case, CPSP was present in the hypalgesic side of face and extremities. In 9 cases of typical type (Currier's distribution of sensory disturbance), CPSP occurred in the ipsilateral face to the lesion during acute stage. Among them, 2 cases developed severe lancinating pain in chronic stage. In 5 cases of ventral type, it occurred in the contralateral extremities during chronic stage. Spino- and trigemino-thalamic tract are injured but medullary reticular formation is intact in Wallenberg syndrome. It is, therefore, considered that CPSP in Wallenberg syndrome is caused by denervation sensitivity of "paleo-reticulothalamic" tract within the reticular formation.

Adult↗
PubMed2004

[Valproate-induced hyperammonemic encephalopathy in a patient with Sjögren's syndrome].

We describe a 56-year-old woman with hyperammonemic encephalopathy caused by side effect of valproic acid (VPA). Ten months before the admission to our hospital, she had the first attack of convulsive seizure. Diagnosis of epilepsy was made, and the oral administration of VPA (800mg/day) was started at another hospital. Seizure was well controlled by VPA, until the recurrence of attack forced her to visit our hospital. Convulsive seizure disappeared immediately after intravenous administration of diazepam, but consciousness disturbance was prolonged for a few days. Since laboratory examinations revealed hyperammonemia without liver dysfunction, VPA was discontinued. Subsequently, her consciousness completely recovered. Other laboratory findings, including positive antinuclear antibody, antibodies to Sjögren's syndrome A, reduced lacrimal secretion in Schirmer's test, and cell infiltration in the salivary gland on lip biopsy specimen, suggested the presence of Sjögren's syndrome. The hyperammonemia occurs by the side effect of VPA, often has basal disease or drug interactions. It was, however, especially in patients with basal disease or other drugs, obscure whether (and how) Sjögren's syndrome contributed to the development of hyperammonemic encephalopathy in this case, since she took only VPA.

Anticonvulsants↗
PubMed2002

Hyperphosphorylated tau deposition parallels prion protein burden in a case of Gerstmann-Sträussler-Scheinker syndrome P102L mutation complicated with dementia.

Hyperphosphorylated tau (p-tau) deposition has been documented in a limited population of patients with Gerstmann-Sträussler-Scheinker syndrome (GSS) with particular point mutations of the prion protein (PrP) gene. Although its pathogenesis is only poorly understood, p-tau in GSS is known to be identical to that in Alzheimer's disease (AD). We conducted immunohistochemical and quantitative image studies on the brain from a 44-year-old man with a 7-year history of dementia, diagnosed as having GSS with a point mutation of the PrP gene at codon 102 (GSS102), the commonest mutation in GSS. Severe spongiform degeneration and numerous PrP plaques were disclosed in the cerebral cortices and hippocampus, consistent with the diagnosis. However, rarely described in GSS102, prominent p-tau deposits as pretangles, neurofibrillary tangles and degenerating neurites were demonstrated adjacent to or around PrP plaques. beta-Amyloid protein (Abeta) plaques were generally sparse and appeared invariably to be of a diffuse type. Double-labeling immunohistochemistry yielded co-localization of p-tau with PrP but not with Abeta. Most PrP plaques did not contain Abeta. These results excluded a diagnosis of concomitant AD. Quantitative analysis on a fractional area density of immunoreactive pixels demonstrated that burdens of PrP and p-tau but not Abeta were significantly correlated. These results suggest that p-tau deposition in this GSS102 is secondarily induced by PrP but not by Abeta (secondary tauopathy). Our study also suggests that p-tau deposition might be a more common phenomenon in long-standing GSS.

Adult↗
PubMed2002

[A case of amyotrophic lateral sclerosis with SIADH and throbbing headache induced by selective serotonin reuptake inhibitor].

A 57-year-old man with amyotrophic lateral sclerosis (ALS) was admitted because of depressive state. Selective serotonin reuptake inhibitor (SSRI), an antidepressant, was started on the admission day. The throbbing headache in the right temporal region appeared on day 3, and an analgesic drug was not completely effective. Serum sodium value on admission was 131 mEq/l. After SSRI was started the hyponatremia rapidly progressed, and it became 112 mEq/l on day 4. SSRI was discontinued, and headache disappeared; serum sodium was improved to 129 mEq/l. It has been reported that syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may be associated with ALS. We consider that subclinical SIADH was manifested by SSRI in this case. SSRI seems to be a cause of headache, since headache disappeared completely by discontinuation of SSRI.

Amyotrophic Lateral Sclerosis↗
PubMed2002

[A study of parasympathetic functions in Guillain-Barré syndrome].

Sympathetic hyperactivity in Guillain-Barré syndrome (GBS) may be due to the involvement of afferent fibers in the vagus and glossopharyngeal nerves within the baroreceptor pathway. Patients with GBS who have increased sympathetic nervous activity, do not, however, always show baroreceptor dysfunction such as orthosatic hypotension. We evaluated parasympathetic nervous activity in patients with GBS to clarity the mechanism of autonomic deficits. An atropine test (20 micrograms/kg intravenous bolus infusion) and hemodynamic functional tests were conducted on 6 patients with GBS (49.5 +/- 13.6 years old) and age-matched healthy controls; 11 controls (50.5 +/- 17.6 YO) for atropine test and 81 controls (48.5 +/- 8.8 years old) for hemodynamic functional tests. I. Parasympathetic nervous activity: (a) Atropine test: (1) Increase in pulse rate after the administration of atropine; the degree was significantly higher in the patients with GBS than that in the healthy controls (p = 0.027). (2) Atropine ratio (= increase in pulse rate following intravenous administration of atropine)/(mean pulse rate before the administration); the ratio was significantly higher in the patients with GBS than that in the healthy controls (p = 0.026). (b) Aschner eyeball pressure test: The degree of reflex bradycardia in the patients with GBS was significantly higher that the in the healthy controls (p = 0.039) II. Sympathetic nervous activity: (a) Cold pressor test: The degree of reflex hypertension was significantly higher in the patients with GBS than in the healthy controls (p = 0.008). (b) 70 degrees passive head-up test: Falls in systolic and diastolic blood pressure in the patients with GBS tended to be lower than in the healthy controls (p = 0.092, p = 0.091). These results suggest that both parasympathetic and sympathetic nervous activities increased, and the baroreceptor function is well preserved in GBS. We thus surmise that increased sympathetic nervous activity in GBS is not explained by reduced inhibition of the parasympathetic nervous activity.

Adult↗
PubMed2002

[A case of Sjögren's syndrome with heat intolerance induced by generalized anhidrosis as its principal feature].

A 60-year-old man was admitted to our hospital because of heat intolerance induced by generalized anhidrosis. There were no abnormal findings on physical and neurological examinations except for anhidrosis. Reflex sweating to pilocarpine and acetylcholine was absent. Skin biopsy revealed no abnormalities of the sweat glands and ducts. Laboratory tests showed elevated levels of serum IgG and rheumatoid factor. Anti-nuclear antibodies, and antibodies to Sjögren's syndrome A and B were positive. Ocular examination revealed the presence of keratoconjunctivitis sicca. The pathological findings of minor salivary gland specimen confirmed a diagnosis of Sjögren's syndrome. This case suggests that generalized anhidrosis could be caused by the antigen-antibody reaction for the cholinergic receptor of sweat gland.

Autonomic Nervous System Diseases↗
PubMed2002

[Serotonin syndrome caused by tandospirone citrate alone].

We describe a case of serotonin syndrome provoked by tandospirone citrate alone, a serotonergic antianxiety agent. A 42-year-old alcoholic woman started to take tandospirone (30 mg/day in 3 divided doses) because of psychosomatic complaints. One month later, dellirium, marked rigidity and myoclonus in the neck and extremities, fever, hyperhidrosis and diarrhoea developed in succession. Tandospirone was discontinued, and all symptoms disappeared within the following 6 days. We diagnosed her condition as serotonin syndrome, although alcoholic withdrawal syndrome might have superimposed. Serotonin syndrome caused by tandospirone alone has not been reported, although it is widely used in Japan.

Adult↗