Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of hemihyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction is reported. A 55-year-old hypertensive man developed right hemiparesis with slight dysarthria and nausea upon awaking. The right side of his face and right upper limb and trunk to the level of the Th8-9 territory showed hyperhidrosis, which disappeared in a week. Ocular motor examination revealed that during forward gaze with the left eye fixing, the right eye deviated outward. The patient was able to adduct the right eye to midposition with the right eye fixing. Rightward gaze elicited full abduction and right-beating nystagmus of the right eye, but the left eye did not adduct. When he attempted to gaze leftward, both eyes made the full excursion, but saccades were slow in that direction. Convergence was intact. Vertical gaze was full, and he did not show Horner's sign. This ocular sign, non-paralytic pontine exotropia, disappeared three days later. T2-weighted spin echo magnetic resonance imaging disclosed a small lesion with high intensity in the inner side of the left middle pons. This hyperhidrosis was thought to be caused by destruction of inhibitory fibers thermoregulating sweating. These findings suggest that at the level of the middle pons inhibitory fibers descend along the inner side of facilitatory fibers thermoregulating sweating, which are speculated to descend the dorso-lateral part of the pontine tegmentum. These findings also suggest that lesions of non-paralytic pontine exotropia may be located in the paramedian pontine reticular formation rostral to the abducens nucleus with ipsilateral medial longitudinal fasciculus lesion, but further investigation is necessary.
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PMID:[A case of hemi-hyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction]. 129 Nov 62

Spontaneous dissections of the internal carotid arteries are uncommon but are not rare. They constitute a fairly common cause of ischemic stroke in young patients (young in terms of the age at which strokes generally occur). The common presenting manifestations are (1) unilateral headaches followed after a period of delay by focal cerebral ischemic symptoms or (2) unilateral headaches and ipsilateral incomplete Horner's syndrome. These may or may not be associated with subjective or objective bruits. In rare instances, spontaneous dissections of the internal carotid arteries may present as lower cranial nerve palsies and cause dysphonia, dysarthria, dysphagia, and numbness of the throat. Affected patients may initially present to the otolaryngologist or be referred to one. This article describes eight patients with spontaneous dissections of the internal carotid arteries and lower cranial nerve palsies, and the pertinent literature is reviewed.
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PMID:Spontaneous dissection of the cervical internal carotid artery. Presentation with lower cranial nerve palsies. 155 74

We report a case of Horner's syndrome due to ipsilateral posterior hypothalamic infarction, occurring in the absence of other signs of hypothalamic dysfunction. Associated symptoms of contralateral faciobrachial weakness and dysarthria correlated with the extension of the infarct into the posterior limb of the internal capsule seen by magnetic resonance imaging. The likely vascular anatomy of this lesion is discussed.
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PMID:Horner's syndrome from hypothalamic infarction. 200 Nov 93

Various types of associated movements of eyeballs with other cranial muscles have been described in the literature. Only a few observations, however, have been reported on the relation of ocular movements and facial muscles innervated by the facial nerve, especially the orbicularis oculi muscles. We report two cases presenting gaze-evoked involuntary contraction of the orbicularis oculi muscle and unilateral eyelid closure. Case 1 was a 38-year-old housewife who was admitted to our hospital because of gait disturbance and sensory deficits below the neck. She had a 5-year history of left facial palsy, disturbed horizontal eye movements, retrobulbar optic neuritis, spastic paraparesis and bladder and rectal disturbances, some of which had relapsed a few times. Neurological abnormalities were summarized as follows: bilateral pale discs, right Horner's sign, horizontal nystagmus, left facial nerve palsy of peripheral type, spastic paraparesis with left-sided predominance, sensory disturbances below the third cervical segment, truncal and limb ataxia, and bladder and rectal disturbances. Gaze-linked synchronized contraction of the left facial muscles was observed and on the left lateral gaze marked spasm of the left orbicularis oculi muscle with occasional lid closure was evoked. Case 2 was a 72-year-old female with cerebellar hemorrhage. Neurological abnormal findings included mild disorientation, meningeal irritation signs, horizontal nystagmus on lateral gaze, reduced response of reflex eye movement to the left, minimal weakness of the left facial muscles, ataxic dysarthria, mild left hemiparesis and hemisensory deficits with face, truncal and limb ataxia. She could move eyeballs to any direction but with effort to the left.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Gaze-evoked eyelid closure. Report of two cases]. 261 99

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration]. 268 32

A case of traumatic occlusion of the bilateral vertebral arteries associated with fracture of the cervical spine is reported. A 34-year-old man, having no previously noted medical problems, fell to the bottom of a bathtub with a depth of 80 cm, and hit the vertex fronto-parietal region of his head. He was transferred to our hospital 6 hours after his fall with a crush fracture of the cervical spine at the C6 level. On admission he was alert, but having pain in the vertex region, dysarthria, blurred vision and hemiparesis. Roentgenograms confirmed a crush fracture of the C6 vertebral body. Computed tomograms of the brain revealed a high density of basilar artery. Cervical traction with a Halo brace was then carried out. Twelve hours after the trauma, left oculomotor and right facial palsy appeared followed by bilateral oculomotor palsy and respiratory difficulty. At the 14th hour, he displayed bilateral Babinski's signs and tetraparesis. Tetraparesis became complete with right-side Horner's syndrome at 16 hours. Cerebral arteriograms performed 20 hours after the trauma showed a complete occlusion of the right vertebral artery and an incomplete occlusion of the left vertebral artery at the C6-7 intervertebral disk space. Conscious level deteriorated to a 200 level on the Japan coma scale 28 hours after the trauma and to a 300 level after 32 hours. Computed tomograms revealed a marked low density on the cerebellum and brain stem 38 hours after the accident. He expired on the 22nd day after the trauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Traumatic occlusion of the bilateral vertebral arteries associated with fracture of the cervical spine--a case report]. 343 47

An autopsy case of Shy-Drager syndrome preceded by urinary disturbance for over 20 years was reported. A 43-year-old woman was admitted to our hospital because of urinary disturbance and orthostatic hypotension. At the age of 19 she developed urinary disturbance with polyuria and retention. These symptoms were getting worse with years, and at the age of 33 she was diagnosed to have neurogenic bladder of uninhibited type. During her hospital course her symptom became worse, and by the age of 42 she showed marked dysarthria, disturbance of smooth pursuit eye movement, Horner's syndrome, marked rigidity and tremor of four extremities, generalized hyperreflexia, marked limb and truncal ataxia, neurogenic bladder and orthostatic hypotension. Serial brain CT scan revealed progressive brain stem and cerebellar atrophy with clinical course. Severe autonomic nervous system dysfunctions were also documented. She died of respiratory failure at the age of 43. On autopsy, brain stem and cerebellum showed marked atrophy macroscopically. Microscopically marked depletion of neuron was seen in the substantia nigra, pontine nuclei, inferior olive, Purkinje cells, the intermediolateral column of spinal cord and Onuf's nucleus of S2. Although numerous cases of Shy-Drager syndrome have been reported in the past, there is no case which developed this syndrome after urinary disturbance of over 20 year's duration. We should be alert to observe the cases with longstanding urinary disturbances in order to not overlook degenerative disorders as exemplified in this case.
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PMID:[An autopsy case of Shy-Drager syndrome preceded by a urinary disturbance for over 20 years]. 382 40

A case of dissecting aneurysm of the cervical internal carotid artery due to rare mechanism by non-penetrating injury is described. A 45-year-old right-handed man had complaints of the right lateral neck pain during exercise of KENDO wearing a tight headneck protector. Following sudden dysarthria and left hemiplegia, he developed loss of consciousness and generalized convulsion. Five hours after admission, he became alert and had no neurological deficits. Four days after these episodes, he loss visual acuity of the right eye, and a few days later he showed left hemiplegia, hypotension, hypersomnia and right-sides Horner's syndrome. Right retrograde brachial angiography revealed so-called "string sign" in the right extracranial internal carotid artery and delayed circulation in the right cerebral hemisphere. He was diagnosed as having traumatic dissecting aneurysm due to blunt (rubbing) injury. He was treated with STA-MCA anastomosis 3 weeks after the accident. Usually, carotid dissecting aneurysm due to blunt injury is produced by hyperextension and contralateral rotation of the neck or direct blow to the neck, but our case shows a possible mechanism of rubbing injury such as simple anteroposterior flexion under tight neck fixation.
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PMID:[Carotid dissecting aneurysm due to blunt (rubbing) injury of the Kendo protector]. 395 67

Clinical features of cerebellar infarction in the territory of the superior cerebellar artery (SCA) were investigated in six male patients, ranging in age from 50 to 69 years. In all patients, there were MR images of infarction located in the area supplied by the SCA. The lesion was on the left-side in 2, right-side in 3 and bilateral (recurrent) in 1 patient. The onset of disease occurred with nausea, vomiting and floating sensation, with no overt brain stem signs other than symptoms of unilateral cerebellar ataxia and dysarthria. Five of the 6 patients had heart disease and cerebral angiography without definite evidence of SCA occlusion, strongly suggesting occlusion of the artery at its periphery due to cardiogenic embolism. A comparison of these 6 patients with those reported previously in Japan suggests that patients with SCA occlusion may be divided into two distinct subgroups: one manifesting diffuse brain stem signs in addition to cerebellar signs, and the other showing cerebellar signs as the only neurologic manifestation. In the former group, comprising the vast majority of patients, SCA occlusion occurred at the origin of the vessel due to a thrombus under a state of hypertension, diabetes mellitus or malignancy, producing signs of brain stem involvement, such as dissociating sensory disturbance and Horner's sign. While in the latter group, which included these 6 patients, paucity of brain stem signs, absence of definite cerebral angiographic evidence of SCA occlusion, and the presence of heart disease were distinguishing clinical features. Cardiogenic cerebral embolism was probably the underlying pathology in many of the cases and the functional prognosis was favorable.
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PMID:[Cerebellar infarction in the territory of the superior cerebellar artery, presenting a predominant cerebellar symptom--with special reference to its pathophysiology]. 761 47

A hemimedullary infarction, in which both medial and lateral medullary infarctions occur simultaneously, is a rare cerebrovascular disease. Pontomedullary lesions often cause central respiratory failure, and the majority of central respiratory failures are due to bilateral pontomedullary lesions. We report a 66-year-old man with central respiratory failure due to a hemimedullary infarction detected by magnetic resonance imaging. He was admitted to our hospital on March 7, 1998, because of a sudden onset of dysarthria, and both numbness and weakness on his left side. Soon after arriving at the hospital, his spontaneous respiration ceased. Therefore, he was intubated and artificial ventilation was started. Pertinent neurological abnormalities on admission consisted of dysarthria, dysphagia, right Horner's sign, right gaze evoked horizontal nystagmus, right soft palate palsy, and tongue deviation to the right. In addition, left hemiparesis, left Babinski's sign, sensory impairment on the left side including the face, and central respiratory failure were noted. Although voluntary respiration recovered in 12 days, sleep apnea continued for 5 months, which was considered to be due to the automatic respiratory failure. An important feature of this patient was that the hemimedullary infarction caused the central respiratory failure. To our knowledge, this is the third patient whose central respiratory failure occurred because of a hemimedullary infarction.
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PMID:[A case report of central respiratory failure due to hemimedullary syndrome]. 1118 17


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