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)

Transient global amnesia (TGA) is an unusual form of the amnestic syndrome, clinically characterized by profound disturbance of short-term memory with preservation of immediate recall and long-term memory. Spontaneous recovery is the rule and is usually complete within several hours. The etiology of TGA is not clear. It is considered to be caused by transient ischemia confined to the medial temporal lobe, an area supplied by branches of the vertebrobasilar system. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff. Besides pulsating headache, the dominant symptoms are vertigo, ataxic gait, tinnitus, dysarthria, paraeshesia in the hands, homonymous hemianopsia and sometimes drop-attacks. These symptoms are associated with vertebrobasilar system dysfunction. In this paper, three migraine patients, suffering from one episode of TGA, were reported. All patients were women. Case 1 was a 48-year-old woman with a history of common migraine. Case 2 was a 48-year-old woman with a history of classic migraine. Case 3 was a 59-year-old woman with a common migraine. Family history of migraine exists in case 1 and case 3. Their migrainous attacks began in their twenties and thirties. They suddenly suffered migraine with the symptoms of vertebrobasilar dysfunction. These symptoms are ataxic gait (Case 1, 2, 3), dysarthria (Case 1, 2), vertigo (Case 1, 3) and homonymous hemianopsia (Case 1, 3). Simultaneously three patients had TGA. Duration of retrograde amnesia were about twenty-four hours (Case 1), about thirty minutes (Case 2) and about three hours (Case 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Basilar artery migraine associated with transient global amnesia]. 262 11

Transient recurrent confusional and stuporous states of nonepileptic origin are clearly less frequent than epileptic ones. They are relatively common in diseases of disturbed vigilance, like narcolepsy, idiopathic hypersomnolence, and sleep apnea. These patients often suffer from attacks of hypovigilance, characterized by altered awareness, automatic behaviour and partial or complete amnesia for the attack. Because of the memory 'black outs' and the frequently associated hypnagogic hallucinations, the patients behave inappropriately and often appear confused. Confusional states also typically arise during basilar artery migraine attacks. This special form of complicated migraine predominantly affects young females and is characterized by symptoms and signs of brain stem dysfunction such as vertigo, ataxia, paresthesia, limb weakness, dysarthria; in 75% of the cases, disorders of consciousness dominate. Transient ischemic attacks are sometimes recurrent and, when involving the cranial basilar territory, may result in confusional states without significant motor dysfunction. Attacks of transient global amnesia are possibly also ischemic in nature and are assumed to arise from transient bilateral limbic failure. Affecting only memory functions, they are strictly spoken not confusional, but must nevertheless be taken into consideration when proper observation during the attack was not possible.
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PMID:[Non-epileptic impaired consciousness in neurologic diseases]. 267 60

Migraine headaches that occur in the 15- to 30-year-old age group are well documented. In patients in the stroke age bracket, however, who present with a history of neurologic deficit, transient ischemic attacks can be confused with migraine accompaniments. The typical patient is 50 years old, is without a past history of migraines, and complains of scintillating visual disturbances (20 percent), marching paresthesis (22 percent), or a myriad of neurologic deficits. In one series of 70 neurology patients aged over 55 years, 16 percent reported that they experience the new onset of scintillations. Once fully evaluated, the cause of unexplained marching paresthesias, dysphagia, or hemiplegia, once reserved for thrombotic or embolic phenomena, may be attributed to migraine accompaniments. In the face of a normal evaluation, neurologic deficit in the stroke age bracket may be attributed to migraine accompaniments. A case of a 47-year-old woman with sudden onset of left-sided paresthesia, dysarthria, and confusion is presented. The discussion includes a description of migraine pathophysiology and a review of concepts regarding accompaniments.
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PMID:Late-life migraine accompaniments: a case presentation and literature review. 358 61

Serotonin syndrome, a condition with numerous clinical neurological manifestations, is the result of central serotonergic hyperstimulation. Features of the syndrome include mental status and behavioral changes (agitation, excitement, hypomania, obtundation), motor system involvement (myoclonus, hemiballismus, tremor, hyperreflexia, motor weakness, dysarthria, ataxia) and autonomic symptoms (fever, chills, diarrhea). Serotonin syndrome has been reported exclusively in patients on medications for psychiatric illness and Parkinsonism, despite the fact that the putative action of many antimigraine agents also involves the serotonin system. We herein report six patients with migraine who developed symptoms suggestive of the serotonin syndrome. Five were taking one or more serotomimetic agents for migraine prophylaxis (sertraline, paroxetine, lithium, imipramine, amitriptyline). In each case the symptoms and signs developed in close temporal proximity with use of a migraine abortive agent known to interact with serotonin receptors. In three instances the agent was subcutaneous sumatriptan and, in three, intravenous dihydroergotamine. In each instance the symptoms were transient and there was full recovery. With the ever increasing use of migraine medications active at serotonin receptor sites, cases of serotonin syndrome will likely occur more frequently. It is important that physicians treating migraine are aware of the serotonin syndrome and are able to recognize its varying presentations.
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PMID:Serotonin syndrome complicating migraine pharmacotherapy. 886 67

Neurological symptoms of transient unsteadiness, dysarthria, dysphasia, dysbasia, transient monoor hemiparesis, hemiparesis, scintillating scotomas, amaurosis fugax, vertigo, dizziness, migraine accompaniments, syncope and seizures were the presenting manifestations of thrombocythemia in various myeloproliferative disorders. Erythromelalgia preceded or followed the neurologic ischemic attacks. The neurologic and ocular attacks usually had a sudden onset, lasted for a few seconds to several minutes and occurred independently or sequentially rather than simultaneously. This clinical syndrome is caused by platelet-mediated ischemic and thrombotic processes in the end-arterial microvasculature and reflects the existence of a platelet dependent and aspirin responsive arterial thrombophilia in thrombocythemia as novel disease entity, which confirms and elucidates Mitchell's hypothesis.
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PMID:Atypical transient ischemic attacks in thrombocythemia of various myeloproliferative disorders. 895 74

Basilar migraine is a complicated headache which the International Headache Society describes as 'migraine with aura symptoms clearly originating from the brainstem or from both occipital lobes'. For years this headache was thought to originate from a transient disturbance in the vertebrobasilar circulation, but more recent studies suggest that a central neuronal disorder may be the source of migraine. Basilar migraines may have certain symptoms which are similar to other neurologic, vascular, psychiatric and metabolic diseases, yet there are specific criteria which can help differentiate it from other diagnoses. It is characterized by a throbbing occipital headache which may be preceded by an aura. The unusual symptoms of basilar migraine, which may precede and continue throughout the duration of the headache and even after it, include bilateral visual symptoms, altered mental status, vertigo, gait ataxia, bilateral paresthesia, bilateral paralysis and dysarthria. We describe a 29-year-old black female whose husband brought her to the emergency department complaining of confusion, headache, and left-sided weakness for 2 h prior to arrival.
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PMID:Basilar migraine. 915 94

We describe a Chinese American family with a hereditary syndrome consisting of retinopathy, nephropathy, and stroke, affecting 11 members spanning three generations. Ophthalmologic evaluations revealed macular edema with capillary dropout and perifoveal microangiopathic telangiectases. Several members had renal abnormalities with proteinuria and hematuria. Initial manifestations were visual impairment and renal dysfunction; neurologic deficits occurred in the third or fourth decade of life. Symptoms included migraine-like headache, psychiatric disturbance, dysarthria, hemiparesis, and apraxia. Neuroimaging consistently demonstrated contrast-enhancing subcortical lesions with surrounding edema. Ultrastructural studies showed distinctive multilaminated vascular basement membranes in the brain and in other tissues, including the kidney, stomach, appendix, omentum, and skin. Genetic analysis ruled out linkage to the CADASIL locus on chromosome 19. Distinct from CADASIL, hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS) is an autosomal dominant multi-infarct syndrome with systemic involvement.
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PMID:Hereditary endotheliopathy with retinopathy, nephropathy, and stroke (HERNS). 937 16

Stuttering is an abnormality in the fluency of speech, which is characterized by interruption of the normal rhythm due to involuntary repetition and prolongation, or arrest, of uttered letters or syllables. The aphasic syndrome and dysarthria can be associated with classic migraine, but, to our knowledge, no study has so far described stuttering as the only neurological symptom accompanying an attack.
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PMID:Acquired transient stuttering during a migraine attack. 1109 4

The neurologic signs and symptoms of carbamazepine and phenytoin toxicity, such as ataxia, dysarthria, and nystagmus, are well known. The psychiatric manifestations of toxicity, such as psychosis and hallucinations, however, are less widely recognized. This study reports the case of a 9-year-old male with seizures who developed intermittent complex visual hallucinations after therapy with antiepileptic drugs was begun. This study considered seizures, migraine, underlying psychiatric diathesis, and drug toxicity as possible etiologies but after extensive investigation concluded that his symptoms were most likely a drug side effect.
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PMID:Antiepileptic drug-induced visual hallucinations in a child. 1111 3

CADASIL disease (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) was described in 1991 by Tourmier-Lasserve. Two years later the same authors described its association with chromosome 19; nonetheless, the mutations in gene Notch3 were not described until 1996. Clinical findings depend on the age at onset. The early form of the illness is found in young patients, generally less than 30 years old, and the main clinical manifestation is a migraine headache with subcortical lesions in the white matter, while in the later form ischemic events and behavioral symptoms are predominant. Anatomo-pathological findings in CADASIL include the presence of osmophilic granular deposits in vessel walls, skin, muscles and cerebral arteries. We present a patient with CADASIL and cavernous angioma. We studied a 40-year-old woman who underwent surgery for a left temporal-parietal cavernous angioma, with aphasia as the only symptom, two years before admission. Her family history showed that her father had suffered from vascular dementia. She was admitted to our hospital with right-side hemiparesis and dysarthria. A CT scan showed the presence of ischemic vascular lesions and former surgery sequelae. The duplex scan of the neck vessels and a transesophageal echocardiogram ruled out an embolic source. Laboratory tests including VDRL, HIV, prothrombotic profile and rheumatologic screening tests were normal. An MRI in T2W and FLAIR showed the presence of multiple subcortical cerebral lesions and hyperintensity in the white matter (leukoencephalopaty). We found a left acute putaminal-capsular infarct in the diffusion-MRI. The MRA was normal. Analysis of the cerebrospinal fluid was unremarkable. A molecular DNA test was performed, and a nucleotide substitution in position 583 in exon 4 of gene Notch3 was detected. This mutation was found only in CADASIL patients. The association with cavernous angioma has not been previously reported, and we believe that it was unrelated to CADASIL, either clinically or genetically. To our knowledge, this is the first case of CADASIL diagnosed by molecular DNA test in our country.
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PMID:[Cadasil: a case with molecular diagnosis]. 1196 50


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