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)

Eight attacks of transient global amnesia were observed in a female patient who suffered from livedo reticularis and a series of other neurological symptoms, which were transient in most stances. The neurological deficits include focal epileptic attacks, unilateral loss of vision, paresis of left arm and/or leg and dysarthria. The first amnestic attack was seen at the age of 19. The episodes lasted from a few to 3 days. The intervals between the amnestic episodes varied between a few days and 11 years. The livedo reticularis became more obvious during each neurological episode and was less pronounced during the time of remission. A benign type of essential hypertension and parproteinemia (gamma-M) was found. The investigations failed to show any evidence of essential thrombocythemia, polyarteriitis nodosa, lupus erythematodes and other immune complex diseases. The underlaying disease remained unclear.
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PMID:Recurrent transient global amnesia in a case with cerebrovascular lesions and livedo reticularis (Sneddon Syndrome). 9 41

An unusual neurovisceral lipid storage disorder in two unrelated juvenile patients manifested itself by dystonia and involuntary movements, with facial grimacing, dysarthria, gait difficulty, and impaired manual dexterity. Supranuclear paresis of vertical gaze and splenomegaly were present. Absent were seizures, major intellectual deterioration, spasticity, or blindness. Histiocytes showed lysosomal storage of various phospholipids, cholesterol, neutral lipids, and autofluorescent material. Appendiceal neurons showed only an increse of phospholipids by histochemistry. Neuronal deposits differed ultrastructurally from these in histiocytes. Leukocyte sphingomyelinase activity was normal. The nosology of this disease and its relationship to so-called juvenile types of Niemann-Pick disease is discussed. The primary metabolic defect in these patients remains unknown.
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PMID:Juvenile dystonic lipidosis: an unusual form of neurovisceral storage disease. 18 51

We report six patients with partial, predominantly paramedian, tegmental pontine hemorrhages. Constant clinical manifestations consisted of: ipsilateral miosis, horizontal gaze paresis, lower motor neuron facial paresis, contralateral hemisensory loss and mild and transitory hemiparesis, dysarthria and mild or no compromise of consciousness. Five out of six were hypertensive. All patients survived with mild sequelae, oculomotor disturbances being the most persistent deficit. We found in our patients that a transverse diameter of less than 17 mm, unilaterality of the injury and absence of coma were the major indicators of a favorable outcome.
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PMID:Tegmental pontine hemorrhages: clinical features and prognostic factors. 162 52

A 32-year old man presented with a bilateral faciobrachial paresis, pyramidal signs in the upper limbs and dysarthria. Computer tomographic (CT-)scans showed bilateral cortical zones of contrast enhancement and strikingly symmetrical capsular hypodensities. Angiography revealed a stenosis of the left internal carotid artery and an occlusion of the right internal carotid artery. Essential thrombocythemia was diagnosed as the underlying disorder. Since there are no indications of pontine lesions, we assume that the signs and symptoms in this patient could mainly be attributed to the bilateral capsular lesions, that resemble lacunar infarcts.
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PMID:Bilateral faciobrachial paresis as a consequence of symmetrical capsular infarcts. 178 Dec 64

A case with non-paralytic pontine exotropia (NPPE) due to brainstem infarction is reported. A 77-year-old hypertensive man suddenly developed dizziness, double vision, dysarthria, and right ataxic hemiparesis. Oculomotor findings on admission consisted of: (1) full right exotropia in the primary position; (2) complete adductive paralysis of the left eye with slight preservation of convergence; (3) tonic deviation of the right eye to the full abducting position with right-beating nystagmus after an immediate forward gaze. The leftward saccades showed multiple saccades with slow velocity on electronystagmography (ENG). The right exotropia disappeared and the slight adductive paresis of the left eye remained with right monocular nystagmus seven weeks after the onset. Magnetic resonance imaging (MRI), which was performed nine weeks after the onset, disclosed a small lesion with high intensity involving the left medial longitudinal fasciculus (MLF) on T2-weighted spin echo image. The leftward saccades showed multiple saccades with normal velocity eleven weeks after the onset. The hypofunction of unilateral PPRF with ipsilateral MLF lesion probably causes the contralateral NPPE.
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PMID:[A case of non-paralytic pontine exotropia due to pontine tegmentum lesion confirmed by magnetic resonance imaging and electronystagmography]. 208 37

We report 5 patients with unilateral infarct and 1 with hemorrhage limited to the genu of the internal capsule. The most prominent finding was contralateral facial and lingual hemiparesis with dysarthria. Three patients also showed unilateral mastication-palatal-pharyngeal weakness, and 1 had unilateral vocal cord paresis. Mild limb involvement was limited to hand weakness in 4 patients. Our findings suggest that the majority of motor corticopontine and corticocobulbar fibers are located in the genu of the internal capsule. The faciolingual syndrome and its variants are highly suggestive of capsular genu stroke.
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PMID:Capsular genu syndrome. 179 70

Four patients with tumours involving or compressing the brain stem are described whose initial clinical symptoms of fluctuating paresis of the external ocular muscles and/or the pharyngeal muscles without other neurological deficits led to the primary diagnosis of focal myasthenia. The combination of an unusual clinical pattern, involvement of muscles of only one ocular nerve or severe dysphagia/dysarthria without extension of the myasthenic symptoms, should lead to further investigation to exclude other reasons of a focal myasthenic syndrome such as a brain-stem tumour.
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PMID:Oculo-bulbar myasthenic symptoms as the sole sign of tumour involving or compressing the brain stem. 227 71

Acute mutism with paralysis of the bulbar and facial muscles following discrete bilateral internal capsular infarction is a rare stroke syndrome. We describe a 62 year-old male who suddenly became unable to speak or swallow. The paucity of facial expression and inability to voluntarily move the facial, lingual and pharyngeal muscles were persistent and contrasted with a relatively mild limb paresis which recovered. High resolution CT scan revealed infarcts in the posterior limbs of both internal capsules. It is important to recognise this stroke syndrome because of the permanence of dysarthria and dysphagia associated with it.
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PMID:Persistent mutism and dysphagia of acute onset due to bilateral internal capsule infarction. 239 43

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

The patient, a man aged 57, was admitted to our clinic on May 1, 1987, because of severe vertigo and unsteadiness in standing. Since the age of 55 he had been suffered from hypertension and atrial fibrillation. In September, 1986, he experienced vertigo but recovered soon without therapy. On April 25, 1987, while working, he noticed severe vertigo, nausea and vomiting. He was admitted to a hospital, and then transferred to our clinic. On admission, he was alert and the mentality was normal. Slight ptosis abducent nerve paresis, hypalgesia on the forehead, nose and cheek, facial paresis of peripheral type and hypacusis were detected on the left side. No anisocoria was observed. Sweating was impaired over the left side of the face. Elevation of the soft palate was limited on the left side and the tongue deviated to the left on protrusion. Dysarthria was detected. Though there was no muscular weakness in the extremities, incoordination and dysmetria were noted in the left arm and leg. He could not stand up because of vertigo and unsteadiness. There was no sensory disturbance in the trunk and extremities. Deep tendon reflexes were well elicited and no pathological reflex was observed. These clinical manifestations, except for the ipsilateral palatal and lingual disturbances, were typical of the lateral inferior pontine syndrome caused by occlusion of anterior inferior cerebellar artery, and the lesion was clearly demonstrated by horizontal and coronal MRI. The palatal and lingual disturbances might be due to the involvements of the corticobulbar tracts of the 10th and 12th nerves after the fibers had decussated.
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PMID:[Lateral inferior pontine syndrome: a case report]. 280 19


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