Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surgical treatment for Parkinson's disease began by blocking of the pyramidal system in early part of this era. In 1942, Meyers performed Ansotomy for the treatment of Parkinsonism without leaving hemiplegia, leading subsequent operating target to blocking of pallidofugal fiber. Then, the development of stereotaxy in 1947 caused an operative progress to Pallidotomy and further to Thalamotomy. Although the spread of levodopa therapy gradually brought about decline of surgical treatment, Thalamotomy became to be reexamined in view of not a little problems about and side effects of levodopa therapy. With the development of CT, MRI and the like, Thalamotomy via MRI-stereotaxy was developed, making operations safer and surer. Besides, transplantation of dopamine neurons into the striatum was tried as an essential treatment and is in clinical application via animal experiments. Fetal ventral mesencephalic tissue and adrenal medullary tissue are available therefore, but demerits are such that the former poses some ethical problem and the latter is poor and short-lived response. The transplantation of stellate ganglion into the striatum, which we have recently developed is safe and more effective than the adrenal medullary tissue. The respective one thirds of the cases did without levodopa following transplantation, needed half as much as the preoperative levodopa dose and needed the same as the latter. Although Horner's syndrome was noted in all cases following transplantation, no Parkinson syndrome became aggravated in any one of the cases.
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PMID:[Surgical treatment of Parkinson's disease]. 827 75

A 20-year-old woman with myelomeningocele presented with acute right-ear pain and right hemiplegia which improved, but then progressively deteriorated. Surgery, after MRI, revealed a large arteriovenous malformation (AVM) involving the right side of the upper cervical cord and brainstem. The woman also had two epidermal nevi at the same site as the spinal cord AVMs. There has been no previous report of an association of myelomeningocele, spinal cord AVMs and epidermal nevi syndrome. The same location of the nevus and spinal cord AVMs, with a proposed common pathogenesis, raise the possibility that the association may be more than chance occurrence. Spinal cord AVMs should be considered in patients with myelomeningocele and similar clinical features.
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PMID:Myelomeningocele, spinal arteriovenous malformations and epidermal nevi syndrome: a possible rare association? 833 63

Two patients with congenital hemiplegia without obvious prenatal, perinatal or neonatal difficulties showed linear low signal intensity lesions along the wall of the dilated lateral ventricles without any parenchymal lesions on T2- and proton density weighted MRI. Haemosiderin deposition secondary to intra-uterine subependymal haemorrhage with intraventricular haemorrhage was considered most likely from the signal intensity, distribution and clinical histories. MRI, which is the only means of detecting haemosiderin deposition, could be beneficial for evaluating the pathogenetic cause of congenital hemiplegia.
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PMID:Periventricular haemosiderin deposition in patients with congenital hemiplegia. 856 49

A 64-year-old man presented with pathologic crying and right hemiplegia due to a unilateral pontine infarct from probable branch disease of the basilar artery. The circumscribed nature of the lesion was supported by MRI and short-latency evoked potentials. The weeping spells ceased after a few days of imipramine in low doses. Pathologic laughing and crying can be viewed as a limbic-motor disconnection syndrome, in which the faciovocal motor system is released from forebrain afferents carrying information of emotional content. The inclusion of pathologic laughing and crying in the syndrome pseudobulbar palsy is inaccurate and misleading, since each is related to distinct functional and anatomic systems intrinsic to the human brainstem.
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PMID:[Pathological crying and unilateral pontine infarction]. 858 32

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64

We report the unusual association of Progressive Facial Hemiatrophy (Parry-Romberg syndrome) with multiple benign tumors (orbital neurinoma, mandibular odontogenous fibroma) and hamartomas. The neurological clinical features were infantile hemiplegia, mild mental retardation and focal seizures. Brain CT-scan and MRI showed porencephaly and cerebral calcifications ipsilateral to hemifacial atrophy. Immunological investigations proved negative. The etiology of the disease and the bridging of this case to phakomatoses are discussed.
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PMID:Progressive facial hemiatrophy with multiple benign tumors and hamartomas. 871 45

We reported a case of cerebral infarction in a young adult following an abuse of cocaine and other drugs. A 27-year-old male was admitted to our hospital because of the abrupt onset of right hemiplegia and dysarthria. Brain CT and MRI examinations showed cerebral infarction in the region of the left caudate head and the left corona radiata. Cerebral angiography revealed total occlusion at the origin of the left middle cerebral artery, with neither vascular malformation nor atherosclerotic change. There were no obvious causes that might lead to cerebral infarction in young adults, including potential cardiac sources of embolism, abnormalities of blood coagulation, or collagen vascular diseases. From his history we learned he had started abusing cocaine and other drugs at the age of 16 years, and that he had been addicted to these drugs up to at least 2 months earlier than the onset of cerebral infarction, so we suggested his drug abuse might have affected the occurrence of cerebral infarction. We would like to emphasize that using 'drugs' should be taken into consideration as a possible cause of cerebral infarction in young adults.
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PMID:[A case of cerebral infarction in a young adult following an abuse of cocaine and other drugs]. 872 Mar 40

A patient with a right internal capsule and thalamic hemorrhage showed ipsilateral hemiplegia. MRI at 10 months after the cerebral hemorrhage demonstrated Wallerian degeneration, which could be traced to the ipsilateral anterior funiculus at the cervical level. The findings of motor evoked potentials and somatosensory evoked potentials indicate a predominantly ipsilateral innervation of motor and sensory systems in this particular patient.
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PMID:Ipsilateral hemiplegia caused by right internal capsule and thalamic hemorrhage: demonstration of predominant ipsilateral innervation of motor and sensory systems by MRI, MEP, and SEP. 944 13

This paper presents a case of traumatic dissection of the unilateral internal carotid artery of the cervical portion caused by hanging. A 63-year-old man attempted suicide by hanging and was rescued immediately after. No neurological deficits were detected for the first 4 hours. But then, right hemiplegia, aphasia and disturbed consciousness suddenly developed. On the 2nd day, MRI revealed multiple infarctions in the left cerebral hemisphere. MR angiography demonstrated severe stenosis at the cervical portion of the left internal carotid artery due to dissection. The left middle cerebral artery was not demonstrated. The patient was conservatively treated with fibrinolytic agents and regained consciousness gradually. But aphasia and right hemiplegia remained. During the next few weeks, the stenosis at the ICA slightly improved and the MCA was completely recanalized. Extracranial Doppler sonography revealed chronological hemodynamic changes of mean flow velocity and pulsatility index at the proximal and distal portion of the ICA stenosis.
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PMID:[Unilateral dissection of the cervical portion of the internal carotid artery and ipsilateral multiple cerebral infarctions caused by suicidal hanging: a case report]. 882 37

Brain abscesses following stroke have been reported only rarely. We presented a case of putaminal abscess following putaminal hemorrhage. The patient was admitted to our hospital because of acute onset of left hemiplegia. The size of the hematoma was medium and the patient was conservatively treated. In about two months after the ictus, he became intermittently febrile and laboratory examinations suggested the presence of general infections including meningitis. Meanwhile, CT and MRI revealed clearly abscess formation at the site of the hematoma with remarkable brain edema. Cerebrospinal fluid analysis showed the findings of meningitis. On diagnosis of brain abscess, stereotactic exploration was performed and pus mixed with old blood was aspirated. Bacteriological study of the specimen demonstrated Morganella morganii. Postoperative course was uneventful and the abscess cavity gradually subsided following drainage and irrigation of the abscess cavity.
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PMID:[Putaminal abscess occurring at the site of hemorrhage: a case report]. 882 38


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