Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
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PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59

Seven patients with mitochondrial encephalomyopathies were studied for peripheral neuropathy by clinical, electrophysiological and pathological examinations. The clinical manifestation of neuropathy varied from asymptomatic to mild and moderate sensorimotor symptoms with painful paresthesia. Five patients (2 with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, and 3 with myoclonic epilepsy and ragged-red fibers, MERRF) had clinical symptoms and signs of polyneuropathy associated mainly with decreased amplitudes of the compound muscle or nerve action potentials in an electrophysiological study indicating axonal degeneration. Sural nerve biopsy from 1 MERRF patient, also confirmed an axonal degeneration with reduction of large myelinated fibers. Mitochondrial DNA analysis of the sural nerve from this patient showed a point mutation from A to G transition at the nucleotide position 8344 with 80% mtDNA mutation. The results of this study suggest that peripheral neuropathy is not uncommon in mitochondrial encephalomyopathies and is predominantly due to axonal degeneration.
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PMID:Peripheral neuropathy in mitochondrial encephalomyopathies. 905 67

Diabetes mellitus associated with mitochondrial tRNA mutation at position 3243(DM-Mt3243) is a new disease. Patients have a distinctly different picture from MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). During observations at the Saiseikai Central Hospital, the following findings were noted in DM-Mt3243 patients: DM-Mt3243 patients are diagnosed earlier with diabetes, compared to NIDDM (non-insulin dependent diabetes mellitus) controls without family history. DM-Mt3243 patients often need insulin more often than NIDDM controls without family history. Post-treatment neuropathy and insulin edema are often found in DM-Mt3243, and the two phenomena possibly have a similar pathophysiology related to mitochondrial dysfunction. Ambiguous psychiatric disorders of functional psychosis are observed frequently in DM-Mt3243. Mild headache is common in DM-Mt3243 cases. Ambiguous neuromuscular abnormalities such as sleep disturbance, paresthesia of the legs, edema of the legs, and palpitation may be symptoms associated with mitochondrial dysfunction in DM-Mt3243. Coenzyme Q may be effective in the relief of these neuromuscular symptoms.
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PMID:Diabetes mellitus associated with 3243 mitochondrial tRNA(Leu(UUR)) mutation: clinical features and coenzyme Q10 treatment. 926 20

Three patients with unusual unilateral sensory disturbances in the thorax, in addition to hand and mouth, hand and foot, and hand, mouth and foot regions, respectively, after stroke, are described. Magnetic resonance imaging (MRI) showed a causative lesion in the ventral posteromedial and ventral posterolateral nucleus of the contralateral thalamus in two patients and the contralateral thalamocortical projections in one patient. Symptoms in three patients were due to infarction. Objective sensory loss was not found, but subjective paresthesia was observed in the thorax, in addition to the hand and mouth, hand and foot, and hand, mouth and foot regions, respectively. Paresthesia recovery time was evaluated in these three patients in addition to seven patients with cheiro-oral syndrome and eight patients with cheiro-oral-pedal syndrome. All thirteen patients who demonstrated recovery showed regional improvement of paresthesia in the following sequences: thorax, foot, mouth and then hand, which suggests that the detection threshold, from highest to lowest, occurs in the following sequences: thorax>foot>mouth>hand. These three cases with thoracic sensory disturbance form the explanatory links between the cheiro-oral syndrome and the cheiro-oral-pedal syndrome; cases with sensory disturbance in the hand, mouth, foot or thorax could be regarded as cases of sensory hemisyndrome in which the subjective experience of symptoms was restricted to the hand, mouth, foot or thorax. These symptoms may possibly be attributable to differential detection thresholds.
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PMID:Unusual sensory disturbance in the thoracic region after stroke: relationship to cheiro-oral and cheiro-oral-pedal syndrome. 945 81

We studied 25 patients with an acute thalamic stroke (infarct or hemorrhage) on CT or MRI scan and sensory dysfunction, among the 3,628 patients with first-time stroke included in the Lausanne Stroke Registry. Twelve patients had a right-sided infarct, 11 a left-sided infarct, and 2 a left-sided thalamic hemorrhage. Sensory symptoms or signs were the only clinical abnormality. The presumed causes of stroke were small artery disease in 21 patients including both cases of hemorrhage, emboligenic heart disease in 2, while the etiology of ischemic stroke was undetermined in 2 patients. Nine patients had a loss of all modalities of sensation with faciobrachiocrural distribution, 5 patients suffered dissociated sensory loss with faciobrachiocrural distribution and 11 patients showed a dissociated involvement of sensation with a partial distribution pattern. The inferolateral region (thalamogeniculate arteries) was involved in all patients. Six patients complained of pain and/or dysesthesias during the stroke; 5 of them had involvement of the nucleus ventrocaudalis (in 3 with damage to the nucleus ventro-oralis intermedius, and in one to the pulvinar) and 1 patient had involvement of the nucleus ventro-oralis intermedius. Eighteen patients complained of paresthesias in the contralateral part of the body; 16 of them had involvement of the nucleus ventrocaudalis (in 4 with damage to the nucleus ventro-oralis intermedius, in 1 with damage to the nucleus ventro-oralis intermedius, and nucleus ventro-oralis externus, and in one with damage to the nucleus parvocellularis and pulvinar). Four patients developed delayed pain and/or dysesthesias; all of them had involvement of the nucleus ventrocaudalis (in 1 with damage to the nucleus parvocellularis and pulvinar). Time lag from stroke onset to developing pain ranged from 2 to 15 days (mean 10.5 days). One patient with dissociated involvement of sensation with a partial distribution pattern had paresthesias and dissociated hemisensory loss involving position sense without pain and temperature sensations. This patient had involvement of the posterolateral part of the nucleus ventrocaudalis. In conclusion, sensory dysfunction and delayed pain are more often found in thalamic lesions that involve the nucleus ventrocaudalis, and nucleus ventro-oralis intermedius. Restricted sensory abnormalities correlate with very small lesions located in critical areas within these nuclei.
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PMID:Pure sensory syndromes in thalamic stroke. 963 71

We investigated the mental health of 47 subjects (30 men, mean age 63.8+/-7.7; 17 women, mean age 68.9+/-8.7) with the 60-item General Health Questionnaire (GHQ). All the subjects lived at home in a Japanese rural community and were examined from 2 to 3 years after suffering a stroke. Among the subjects, 18 (38.3%) had GHQ scores of 17 or more, which indicated a mental health problem (MHP). The following variables were included in multiple logistic regression analysis: age, sex (men/women), grade of motor paralysis (no/slight/moderate/severe), side of motor paralysis (no/left side/right side/both sides: in analysis, we used dummy variables), paresthesia (no/yes), rehabilitation (need no rehabilitation or participate in rehabilitation/fail to participate in rehabilitation), social support (not needed or sufficient/insufficient) and overall physical recovery (1/2/3: 1 = 67-100, 2 = 34-66, and 3 = 0-33 on a visual analog scale 100 mm long, 100 meaning full recovery). In univariate analysis all variables except age and sex showed statistically significant associations with MHP. In multivariate analysis, only one variable, overall physical recovery', had a statistically independent association with the status of MHP (Odds ratio 4.39, 95% confidence interval 1.46-13.19). The results of logistic regression analysis indicate that the presence of an MHP is more strongly dependent upon subjective assessment about overall physical recovery after stroke than upon physical impairments and the other psychosocial variables. Therefore, in the community setting, the visual analog scale of overall physical recovery is considered to be a simple, valid method for assessing MHP following stroke.
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PMID:Mental health problems after stroke. 1068 41

Patent foramen ovale (PFO) is a frequent condition which carries a significant risk for stroke when associated with deep venous thrombosis and primary or secondary coagulation abnormalities. Here, we describe a patient in which scuba diving is thought to be associated with stroke in a subject with an otherwise clinically silent PFO. During a rapid ascent a 43-year-old-scuba diver reported weakness and paresthesias in the right arm which lasted about 10 min. He presented similar symptoms 2 days later 1 h after diving, and a third time on his flight back home. The MRI showed multiple hyperintense areas on T2-weighted images in the white matter. Transoesophageal echocardiography (TEE) showed a PFO, whilst all haematological and haemocoagulation tests were negative. Scuba diving may constitute a patho-physiological condition in the presence of PFO as breath-holding promotes right-to-left shunt and arterialization of venous bubbles.
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PMID:Stroke in a scuba diver with patent foramen ovale. 1178 82

A 7-year-old male presented sudden-onset left hemiparesis, left-sided paresthesia, central paralysis of the left VII cranial nerve, and subsequent headache. Magnetic resonance scans were obtained 24 hours after admission. T(2)-weighted images disclosed hyperintensities located mainly in the posterior portion of the lenticular nucleus and in the head and body of the right caudate nucleus. A diagnosis of ischaemic stroke was made on the basis of neuroradiologic findings. Laboratory tests undertaken to establish the cause of stroke revealed parvovirus B19 infection preceding the neurologic abnormalities. In the absence of other known risk factors for stroke the possibility of parvovirus B19's being correlated with stroke onset is discussed.
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PMID:Case of stroke in a 7-year-old male after parvovirus B19 infection. 1265 25

Neuropathic pain is a clinical entity designating the different types of pain associated with a lesion of the nervous system including a wide range of pathological conditions from painful peripheral lesions (for example diabetic neuropathy, post-zoster pain, trauma-induced nerve injury) and central pain (particularly stroke-induced pain, spinal lesions, and multiple sclerosis). Despite this wide range of etiologies, neuropathic pain has well characterized clinical features which generally allow distinction from other types of pain: continuous often burn-like pain, paroxysmal pain (electrical discharge, knife stab), evoked pain, highly invalidating pain (allodynia, hyperalgesia), and associated dysethesia and/or paresthesia. Over the last ten Years, very little work has been published on neuropathic pain, which is now becoming a very active domain of research in neurobiology. Advances to date have not been spectacular although better tolerated agents have been recently marketed. Future progress should enable an appropriate response to the therapeutic challenge of neuropathic pain.
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PMID:[Neuropathic pain: experimental advances and clinical applications]. 1503 77

A 44 years old female was admitted with previous history of several cerebral vascular accident (CVA). A transthoracic echocardiogram showed a patent foramen ovale (PFO) that was closed, under extracorporeal circulation. The patient remained free of symptoms for ten years. In the year 2003 she was admitted to our hospital with paresthesias of the left arm. The clinical evaluation led to the diagnosis of arteriovenous fistula (AVF) of the lung. In November 2003, the patient underwent right inferior lobectomy. This is a rare association of PFO with AVF fistula of the lung with a delayed diagnosis. The differential diagnosis, the surgical treatment and the most frequent complications of this pathology are reported and discussed.
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PMID:[Pulmonary arterio-venous fistula: a clinical report]. 1519 Apr 7


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