Parkinson's disease following panic disorder.
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Biomedical subjects
Publications and source records attributed to Masakuni Kameyama.
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The objective was to compare brain perfusion image using 3-dimensional stereotactic surface projection analysis of N-isopropyl-p-123I iodoamphetamine single photon emission computed tomography between Parkinson's disease patients with a high frontal assessment battery score and those with a low frontal assessment battery score. Thirty nondemented patients with Parkinson's disease were studied. Patients were divided into 2 groups: a high-scoring group whose frontal assessment battery score was 12 or more and a low-scoring group whose frontal assessment battery score was 11 or less. The high-scoring group included 21 patients, and the low-scoring group included 9 patients. They underwent N-isopropyl-p-123I iodoamphetamine single photon emission computed tomography, and we analyzed the data by the 3-dimensional stereotactic surface projection method. Results showed that left inferior parietal lobule and left supramarginal gyrus perfusion of the low-scoring group were significantly decreased compared with the high-scoring group. It is concluded that patients with Parkinson's disease may have frontal lobe dysfunction, but the decreased frontal assessment battery score may be caused not by progressed frontal lobe dysfunction but by parietal lobe dysfunction added to their preexisting frontal lobe impairment.
Pathophysiology of hallucinations in Parkinson's disease is poorly understood. This study investigated relationships between visual hallucinations and visual acuity. Twenty-six consecutive patients with Parkinson's disease participated in this study. Patients were divided into two groups: patients with visual hallucinations (VH group) and those without visual hallucinations (no-VH group). Unaided and corrected eyesight was evaluated in all patients, and if frequent use of prescription glasses or contact lenses was involved, eyesight using these lenses was also measured as the patient's own best eyesight. If a patient did not use prescription glasses or contact lenses, the patient's own best eyesight was defined as the unaided eyesight. Multivariate regression analysis demonstrated that agonist use and best eyesight were different after the backward elimination method. Visual hallucinations were closely related not to uncorrected eyesight or unaided eyesight but to the patient's best eyesight. It is suggested that impaired visual acuity is a risk factor for visual hallucinations.
We described a 69-year-old woman with neurological manifestations due to mixed connective tissue disease (MCTD). The patient demonstrated subacute cognitive decline, seizure and gait disturbance with no connective tissue manifestation. She had been diagnosed with dementia at another hospital, later in our hospital, serological examinations disclosed high titers of anti-RNP antibody. Cognitive dysfunction in this patient was dramatically ameliorated by steroid therapy. Three months later, she developed edema of the hands, synovitis and acrosclerosis. The patient was finally diagnosed as having MCTD. We emphasized MCTD as a rare cause of "treatable dementia".
We investigated the clinical efficacy and tolerability of 45 mg/day mosapride, a selective 5-hydroxytryptamine type 4 (5-HT4) agonist, in an open-label study involving five patients with Parkinson's disease (PD) who had response fluctuations (RFs). 'On' time and motor function scores were determined, and gastric motility was measured by a radionuclide gastric emptying (GE) test, the most reliable quantitative method available. We found that mosapride therapy significantly shortened GE half-time, reduced RFs, and improved motor functions in all patients. There were no adverse reactions. We conclude that selective 5-HT4 agonist therapy is beneficial for patients with PD who have RFs.
We compared MIBG uptake at various parts of the body in controls and patients with Parkinson's disease and multiple system atrophy. In the heart, MIBG uptake in Parkinson's disease (early H/M: 1.668+/-0.325, late H/M: 1.500+/-0.402) was less than that in multiple system atrophy (early H/M: 2.395+/-0.186, late H/M: 2.530+/-0.391) and controls (early H/M: 2.635+/-0.508, late H/M: 2.575+/-0.635) (early: P<0.0001, late: P<0.0001). There were no significant differences in uptake by the lung, thyroid, or liver in the three groups. Only on early images, uptake in the shoulder in multiple system atrophy (early S/M: 0.473+/-0.78) and Parkinson's disease (early S/M: 0.470+/-0.710) was decreased compared to that in controls (early S/M: 0.560+/-0.118) (P=0.0252). MIBG is reported to be taken up in the terminal part of sympathetic nerves and demonstrates sympathetic nerve activity, especially on late images. The cause of differences between the heart and other parts of the body remains unknown. We consider the following possibilities: (a) differences in the sympathetic nervous system between Parkinson's disease and multiple system atrophy are more subtle in organs other than the heart; (b) the cause of MIBG uptake reduction by the heart in Parkinson's disease involves factors in addition to sympathetic nervous system damage; and (c) MIBG uptake by organs other than the heart involves not only the sympathetic nervous system but also non-neuronal components. In conclusion, MIBG uptake by organs other than the heart cannot differentiate Parkinson's disease from multiple system atrophy at present.
Gait disturbance is a cardinal symptom in patients with Parkinson's disease. Among the gait disturbances, freezing of gait is a unique and troublesome symptom, but its mechanism is unclear. We compared brain perfusion images using three-dimensional stereotactic surface projection analysis of N-isopropyl-p-123I iodoamphetamine single photon emission computed tomography between Parkinson's disease patients with freezing of gait and those without. Twenty-four cases (freezing of gait group) with Parkinson's disease with freezing of gait, and 31 Hoehn and Yahr stage-matched cases (no freezing of gait group) with Parkinson's disease without freezing of gait were studied. Bilateral Brodmann area 11 perfusion of the freezing of gait group decreased significantly compared to that of the no freezing of gait group. The Brodmann area 11 may play important roles in gait, and impairment in this region may have a close relationship with freezing of gait in Parkinson's disease.
BACKGROUND: Decreased cardiac metaiodobenzylguanidine (MIBG) uptake was reported in Parkinson's disease and this contributes to the differential diagnosis between Parkinson's disease and other forms of parkinsonism such as multiple system atrophy. However, decreased MIBG uptake of the thyroid has not been demonstrated. OBJECTIVE: To compare MIBG uptake of the thyroid among Parkinson's disease, multiple system atrophy and controls. METHODS: Twenty-six patients with Parkinson's disease, 11 patients with multiple system atrophy and 14 controls were examined in this study. Planar images were taken 15 minutes (early images) and 3 hours (late images) after intravenous injection of 111 MBq 123I-MIBG. RESULTS: MIBG uptake of the thyroid on early images decreased significantly in Parkinson's disease compared to controls (p < 0.0001) and multiple system atrophy (p = 0.018). MIBG uptake of the thyroid on early images decreased significantly also in multiple system atrophy compared to controls (p = 0.027). On late images, thyroid uptake differed significantly only between Parkinson's disease and controls (p = 0.010). CONCLUSIONS: Our study is the first to demonstrate decreased MIBG uptake of the thyroid in Parkinson's disease. Sympathetic nervous denervation of Parkinson's disease occurred not only in the heart but also in the thyroid.
BACKGROUND: The patterns of regional cerebral blood flow in Parkinson's disease and multiple system atrophy remain inconsistent. OBJECTIVES: To compare brain perfusion images of 123I-IMP SPECT between Parkinson's disease, multiple system atrophy with predominant parkinsonian features (MSA-P) and controls. METHODS: Eighty-two patients with Parkinson's disease, 10 patients with MSA-P and 14 controls were studied. We performed 3D-SSP and volume of interest analysis using 123I-IMP scintigraphy. RESULTS: Occipital perfusion of MSA-P increased compared to that of Parkinson's disease and perfusion in the cerebellum and primary sensorimotor cortex of Parkinson's disease increased compared to that of MSA-P. Perfusion in the putamen of MSA-P decreased compared to that of Parkinson's disease. CONCLUSION: Our study demonstrated perfusion differences in 123I-IMP SPECT between the two diseases.
BACKGROUND: Intellectual deterioration occurs in 10-40% of patients with Parkinson's disease. However, there are many conflicting studies on its relation with brain perfusion and the nature of this dementing process remains controversial. OBJECTIVE: To compare cortical perfusion by SPECT using (123)I-IMP between Parkinson's disease patients with dementia and those without dementia and to investigate the correlation between dementia in Parkinson's disease and brain perfusion in various areas. METHODS: Fifty-two cases of Parkinson's disease and 10 control cases were studied. The Parkinson's disease with dementia group included 30 cases and the Parkinson's disease without dementia group included 22 cases. RESULTS: By multiple logistic regression method, we demonstrated significant hypoperfusion in the occipital cortex in Parkinson's disease with dementia. CONCLUSIONS: The cause of dementia in Parkinson's disease may vary. We demonstrated that occipital hypoperfusion was closely correlated to dementia in Parkinson's disease compared to frontal, parietal and temporal perfusion.
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A 27-year-old woman was admitted to our hospital with tetraparesis, dysesthesia and hypoesthesia of all regions below the breasts, urinary disturbance, and difficulty in breathing. Since age 21 idiopathic thrombocytopenic purpura (ITP) was diagnosed and steroid therapy was continued. At age 26, she had splenectomy for her ITP. On admission, steroid pulse therapy was administered with a tentative diagnosis of transverse myelitis. Symptoms gradually ameliorated. At age 29, she gradually lost her left vision, and multiple sclerosis was diagnosed and steroid therapy was administered, and her left vision gradually ameliorated. There are several reports describing other autoimmune disorders that arise after splenectomy. Since the spleen acts as a major pool of type 2 helper T cells, it is plausible that peripheral type 1 helper T cell activity may increase after splenectomy, promoting the development of autoimmune disorders. We considered there would be a close relation between splenectomy for ITP and multiple sclerosis in this case.
POEMS syndrome is a syndrome that presents with polyneuropathy, organomegaly, endocrinopathy, M-proteins and skin changes. Elevated vascular endothelial growth factor (VEGF) has recently been reported in POEMS syndrome. We report a case of POEMS syndrome with high VEGF titers. Steroid, plasmapheresis and intravenous gamma-globulin had little effect. Various immunosuppressive agents were discontinued due to side effects. Although administration of aspirin did not decrease VEGF, ticlopidine decreased VEGF significantly. This case suggests that ticlopidine is a candidate for supportive therapy in POEMS syndrome and we should measure VEGF before and after the administration of ticlopidine in other cases.
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We report two cases of Parkinson's disease in which visual hallucinations disappeared after cataract surgery. Patient 1 was a 72-year-old woman with Parkinson's disease, visual hallucinations and musical hallucinations. Patient 2 was a 77-year-old woman with Parkinson's disease and visual hallucinations. Both patients had severe bilateral cataracts. Though it was difficult to control their visual hallucinations with medication only, cataract surgery made them disappeared quickly. The visual hallucinations of Parkinson's disease are similar to those of Charles Bonnet syndrome. For example, both hallucinations often happen in dim light, at night and when patients are awake with eyes open. Though there have been many reports describing visual hallucinations in Parkinson's disease, there have been few reports discussing the relation between these hallucinations and impaired visual acuity. Similar to the hallucinations of Charles Bonnet syndrome, impaired visual acuity should be related to the visual hallucinations of Parkinson's disease. When Parkinson's disease, visual hallucinations and severe cataract coexist, visual hallucinations may disappear after cataract surgery.
A 50-year-old man who first noticed shaking of the hands at age of 18 and had previous history of three convulsive episodes was admitted to our department because of the generalized tonic seizure with loss of consciousness. Family history showed that 7 members had similar shaking and one had generalized seizure. On neurological examination, rhythmic myoclonic jerks were noted in the bilateral upper limbs, and was remarkably more severe on the left. Other neurological findings were normal. Based on the benign clinical course, familial history, and the normal range of pyruvate and lactate levels in serum and cerebrospinal fluid, we diagnosed familial essential myoclonus and epilepsy (FEME)/benign adult familial myoclonic and epilepsy (BAFME). After admission, we performed electrophysiological test. EEG showed spike discharge mainly in the left parietooccipital lobe. Jerk-locked back averaging (JLA) showed spikes 30 msec precedings the trigger in the left parietooccipital lobe. Because JLA spikes are commonly found 20 msec precedings the trigger, we consider the subtraction time of 10 msec was due to the conduction through the corpus callosum. Some reports showed that in progressive myoclonus epilepsy patients, transcallosal excitation of one hemisphere by the other was critical for generalized seizure. In cases of FEME/BAFME, epileptic focus in the hemisphere ipsilateral to the myoclonus limbs has not previously reported. Our case suggested that generalization of the seizure was caused by the interhemispheric excitation through the corpus callosum.
We report a 65-year-old woman with sudden onset of paresthesia on the left side of the lip and left thumb. Neurological examinations did not demonstrate any disturbance of higher brain function or motor function except for subjective thermohyperesthesia of the left thumb. Brain MRI demonstrated a small high intensity lesion on T2-weighted images (T2 WI) and diffusion-weighted images (DWI) in the right anterior precentral gyrus. She was diagnosed with cerebral infarction presenting with pure cheiro-oral syndrome (COS). Her neurological symptoms were completely abolished 4 or 5 days later. The thalamus is the region responsible for COS in the majority of cases while reports that a cortical infarction causes COS are rare, because it is difficult to show a small cortical lesion on CT or conventional T2WI. DWI is superior to T2 WI in discriminating between acute and chronic ischemic lesions as well as in detecting small cortical lesions adjacent to the cerebrospinal fluid. In this patient, the lesion was vaguely hyperintense on T2 WI and difficult to differentiate from an artifact caused by cerebrospinal fluid. The precentral gyrus infarction detected on DWI was thought to cause COS in this patient. Not only lesions of the postcentral gyrus as a primary sensory cortex but also those of the precentral gyrus or opercula causing COS were described in previous reports, indicating that the hand and mouth sensory areas may be widely distributed. Cortical mapping studied by electrical stimulation through subdural grid electrodes also supports this finding. Further examination of the relation between neurological symptoms and localization on MR images such as DWI is needed to clarify the distribution of the sensory cortex.
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