Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year old woman with a history of recurrent goiter, who had undergone two partial thyroidectomies, is described. She presented with tachycardia, nervousness and a fine tremor of the fingers. Initially, she had normal serum thyroid hormone levels: thyroxine (T4 (D)) 11.6 MUG/100 ML, TRIIODOTHYRONINE (T3) 138 ng/100ml, normal levels of binding proteins and a very high serum thyrotropin (TSH), 98 muU/ml. During follow-up T4 (D) increased to 17.2 mug/100 ml, T3 increased to 277 ng/100 ml, while TSH decreased to 11 muU/ml. There was an exaggerated response of TSH to a peak value of 550 muU/ml after intravenous administration of 200 mug thyrotropin-releasing hormone (TRH). Administration of 60 mg prednisolone daily resulted in a blunting of the response to TRH. Administration of 50 mug T3 daily for 1 month resulted in a fall in serum TSH from 98 to 50 muU/ml. Later, when the serum TSH level had fallen spontaneously to 20 muU/ml, administration of 100 mug T3 daily for two weeks resulted in a fall in serum TSH to 5.3 muU/ml. Treatment with 20 mg carbimazole daily for 3 weeks resulted in a decrease in serum T4 levels with a concomitant increase of serum TSH. There was no evidence of pituitary enlargement and other pituitary hormone levels were normal. All the relatives studied (father, sister, three children) had elevated T4 levels with normal basal TSH values. It is concluded from this study that our patient presents evidence of partial resistance to thyroid hormones.
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PMID:Familial partial target organ resistance to thyroid hormones. 6 Mar 46

H. I., a housewife aged 55 years, began feeling a gait disturbance at 48 years old. After this she had incoordination of arms, dysarthria and tremor of hands. Aged 54 years, she could not stand up by herself. In addition to these neurological signs she had a change of character, such as losing control of herself, unreservedness and unceremoniousness, and slight disturbance of intelligence. She died at the age of 55 years about seven years after the onset. Histopathologically, noticeable changes were observed on the medulla oblongata, pons and cerebellum; the severe neuronal loss of the pontine nuclei and the olivary nuclei with demyelination and gliosis of the cerebellopetal fibers. Especially a great deal of lipofuscin granules in the nerve cells of the frontal and temporal lobe were observed. In the substantia nigra some pigmented cells were deleted. This case was diagnosed as olivo-ponto-cerebellar atrophy clinico-histopathologically. We discussed conserning the etiology of the changes of personality and slight disturbance of intelligence in relation to histopathological changes. It is speculated that the mental disorders are due to the degeneration of the nerve cells in the frontal and temporal lobes.
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PMID:[Olivo-ponto-cerebellar atrophy with personality changes and slight disturbance of intelligence]. 103 31

A case with cortico-basal degeneration was reported with special reference to the immunohistochemical study. A 59-year-old housewife noted tremor and clumsiness of her left hand. On the initial examination she showed the hyperreflexia of the upper extremities and jaw jerk, parkinsonian symptoms such as Myerson sign, parkinsonian gait and rigidity in the left arm. She showed pronounced forced grasping in the left hand. At the age of 60 she showed a WAIS scale with verbal IQ of 99 and performance below the scale. She could not copy hand postures. Tremor was aggravated by action or anxiety, more prominent on the left hand. There was some incoordination on the finger-nose testing of left arm and on the knee-heel testing of both legs. She also showed homolateral dyskinesia. She had a left Babinski sign and sensory testing was normal. A CT scan showed slightly enlarged ventricles (Fig. 1). At the age of 61 she could not understand simple requests and speak few words spontaneously, showing severe dysarthria. There were palilalia and motor impersistence. CT scan showed more widening of the lateral ventricles. At the age of 62, she had lingual dyskinesia and tapping on her upper lip provoked myoclonic jerk on her arms. She died of pneumonia at the age of 65 years, 6 years from the onset. The brain weighed 1190 g. There were bilateral old subdural hematomas on the right parietal and occipital lobe and the left parietal lobe. There was atrophy of frontal and superior parietal region.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Widespread tau abnormality in a case of cortico-basal degeneration]. 129 53

Panic attacks occur more often in females than males with onset usually in the late 20s. A 27-year old woman who experienced a panic attach (heart palpitations, fatigue, bodily shaking, labored breathing, and feelings of terror and being out of control) after she stopped taking a combined oral contraceptive (COC) (.5 norgestrel and .05 mg ethinyl estradiol) was admitted to Osaka Medical College in Takatsuki, Japan. She experienced depression at 18 and took limited amounts of antidepressants for only 1 year. When she started taking the COC at 27, she experienced feelings of unreality and fear, hyperventilation, and heart palpitations. Laboratory results showed lower than normal levels of plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) and a low estradiol level. Yet the plasma cortisol level was much high than normal (22.5 mcg/d1 vs. 3-15.2 mcg/d1). Administration of 200 mg sulpiride/day and 1.2 mg alprazolam/day alleviated almost all symptoms. She did experience mild phobic avoidance and anxiety, however. After successful treatment in the hospital, she discharged herself. Because she was concerned that the panic attacks would recur, she was provided with information on her disorder. She agreed to continue the medication. 1 possible explanation for this case is rapid endocrinological change induced by the ingestion and stopping of the COC which in turn induced a sympatho-adrenal response (her high cortisol levels) to several simple physiological stimuli. Another possible explanation is the COC induced rapid endocrinological changes that may have brought on an anxiotropic effect in someone who had earlier experienced depression.
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PMID:A case of panic disorder induced by oral contraceptive. 131 8

We reported a 65-year-old man whose sister was suffering from HTLV-I-associated myelopathy (HAM) and who presented slowly progressive spastic paraparesis, sensory disturbance in the feet, tremors and cerebellar ataxia. He was also positive for serum anti-HTLV-I antibody. He first showed a head tremor at the age of 3 years. He developed a spastic and ataxic gait when aged 15 years, and it became difficult for him to walk at the age of 50 years. Examination at 65 years showed a spastic and ataxic gait and scanning speech. Hyper-reflexia and Bahinski's signs were observed. Sensation in the feet was decreased. The anti-HTLV-I antibody titer in the serum was 1:512 by the PA method, and Western blot analysis revealed bands of P19, P24, P28 and P32. Examination of the cerebrospinal fluid (CSF), including oligoclonal bands, gave normal results. The CSF was negative for anti-HTLV-I antibody. CT and MRI of the head showed cerebellar atrophy. His sister was 60 years old. She had developed a spastic gait at the age of 15 years. Sensory defects and bladder dysfunction developed when aged 35 years. Hyper-reflexia, Babinski's sign and foot clonus were observed. Sensation in the feet was decreased. The urinary residual volume was increased. Ataxia was not observed. The anti-HTLV-I antibody titer in the serum was 1:8,192 by the PA method, and Western blot analysis revealed bands of p24, p28 and p32. Examination of the CSF, including oligoclonal bands, gave only normal results.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spastic paraparesis and sensory disturbance improved by prednisolone therapy]. 139 32

We report a 72-year-old woman who showed marked orolingual dyskinesia and choreoathetoid movements of the neck, with rolling and nodding of the head. She had been treated for postural tremor and other complaints with multiple drugs, including trihexyphenidyl HCl (THP) 6 mg/day for about two years. Moreover, two months before admission to our hospital, a doctor added tricyclic antidepressant, dosulepin HCl (DL) because of her state of anxiety. Two weeks following DL administration, the persistent dyskinesia described above appeared. Suspecting the dyskinesia to be induced by anticholinergics, we withdrew THP, which decreased the intensity of the dyskinesia. Then, when DL was ceased the dyskinesia almost completely disappeared, slightly recurring only during calculating, when excited or writing. In order to confirm that anticholinergics were the cause of the dyskinesia, we administered THP 6 mg/day again. In a few days the same dyskinesia reappeared, disappearing following THP withdrawal. In this case the overlap of anticholinergics might have resulted in the dyskinesia, because both THP and DL have anticholinergic effects. It should be stressed that inappropriate administration of anticholinergics could cause severe dyskinesia in the elderly.
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PMID:[A case of choreoathetoid movements induced by anticholinergic drugs, trihexyphenidyl HCl and dosulepin HCl]. 143 66

A 21-year-old woman was admitted with right hemiballism and tremor. She had tremor since the age of 6 years. At age 12, an intracerebral, left paraventricular space-occupying lesion was found and treated with 4,500 rads. Increasing tremor was associated with mass enlargement. By age 20, there was insidious presentation of right hemiballism. At age 21, she had craniotomy and a large septate cyst was opened and drained. Biopsy of the cyst wall revealed that it was consistent with ependymal cyst. Postoperatively the hemiballism resolved and the tremor improved. This case is unusual due to the presentation of hemiballism caused by ependymal cyst.
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PMID:Hemiballism and tremor due to ependymal cyst. 148 35

A 53-year-old woman developed symptoms of slow speech, mild dementia, increased deep tendon reflex, ataxic gait, flapping tremor, and dystonic posture during two years. She had liver cirrhosis and hyperammonemia, which suggested a diagnosis of portal-systemic encephalopathy. MR T1-weighted images showed increased signal intensity in globus pallidus, internal capsule, substantia innominata, and a part of hypothalamus. T2-weighted images revealed abnormal findings as follows: high intense area in middle cerebellar peduncle, and low signal intensity of corpus callosum and pontine base. This is the first report about MRI abnormalities in substantia innominata, corpus callosum, and pontine base in a patient with portal-systemic encephalopathy.
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PMID:[A case of portal-systemic encephalopathy presenting characteristic MR images in globus pallidus, hypothalamus, corpus callosum, pontine base, and middle cerebellar peduncle]. 161 82

A Japanese woman, aged 42, was admitted because of paroxysmal attacks consisting of paresthesia of the left face, tremor in the right hand, epigastric pain and urinary incontinence. A year prior to the admission, she noticed some difficulty in writing, dysarthria and unsteadiness of walking. These symptoms had been persistent since then. At the end of March, 1991, these symptoms rapidly worsened, and she fell down frequently. She also experienced pain behind both eyes, numbness in her left fingers and toe, urinary frequency and the above-mentioned attacks. Neurological examination disclosed bilateral internuclear ophthalmoplegia and upbeating nystagmus on upward gaze, titubation in the head, scanning speech, dysmetria in all limbs, exaggerated reflexes in jaw and both legs, bilateral extensor plantar reflexes and ankle clonus. SEP showed delayed cortical response with stimulation of the median nerves bilaterally and of the right posterior tibial nerve. P40 was absent with the left posterior tibial nerve stimulation. VEP was normal. T2-weighted image of MRI showed multiple high intensity areas located around the third ventricle, crus cerebri and the right upper part of the pons. The diagnosis of multiple sclerosis was made. Each paroxysmal attack started with numbness in the left face and burning sensation in the neck. Almost simultaneously tremor in the right hand began. The surface EMG showed the rhythmic contractions in the dorsal hand muscles and wrist extensors at a frequency of 6-7 Hz, and sometimes it revealed synchronized contractions of finger flexors and the dorsal hand muscles. A few seconds later she felt painful sensation in the epigastric region, and the tremor gradually increased in its intensity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of multiple sclerosis with paroxysmal attacks of facial paresthesia, unilateral hand tremor, epigastric pain and urinary incontinence]. 162 36

We report an autopsy case of a 73 year-old female with idiopathic parkinsonism, characterized pathologically by the wide spread appearance of Lewy bodies (LBs) not only in the pigmented neurons in the midbrain and brainstem but also in the cerebral cortex. Initial symptoms at the age of 62 were finger tremor and gait disturbance, which were followed mainly by mental deterioration, such as regression, dependency, auditory hallucination, depression, emotional incontinence, and a personality change. In the terminal stage, nuchal stiffness in extension, one of the hallmarks of progressive supranuclear palsy, and slow and generalized tremor in all 4 extremities were noted. She died of aspiration pneumonia. The brain was somewhat small and weighed 1100 g after the fixation by formalin. Macroscopical findings included mild cerebral atrophy with mild pial thickening both in the frontal and temporal lobes and slight expansion of the ventricular system. Histopathologically, severe loss of neuronal cells in both the pallidum and Luy's body and moderate loss of large cells in the putamen were noted in addition to the typical findings of Parkinson's disease in the substantia nigra and locus caeruleus including neuronal cell loss, depigmentation, and gliosis. These findings in the basal ganglia were more conspicuous than the two controls of classical Parkinson's disease. The distribution, stainability in the routine methods of staining, and shape of Lewy bodies in the cerebral cortex conformed to those of previous reports. The similar case reports in the literatures do not seem to have paid much attention to the findings of the basal ganglia observed in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of idiopathic parkinsonism with numerous Lewy bodies in the cerebral cortex--diffuse Lewy body disease]. 165 48


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