Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The syndrome of chronic vertebrobasilar insufficiency (VBI) consists in a complex of symptoms, often mild and transient, and lacks a complementary system of objective paraclinical investigations able to certify its existence. The study of somato-sensory, auditory and visual evoked potentials in VBI showed the occurrence of changes regardless of the symptom importance both in disorders due to extrinsic causes: a) compression by a damage of the cervical column (92.9%, 50% and 63.9%, respectively; b) diseases of the cervical spinal cord (92.9% and 46.6%, respectively) and in disorders due to some intrinsic vascular causes such as atherosclerosis (62.5%, 88.8% and 87.5%, respectively). We described: a) local and far field modifications for the somesthetic evoked potentials (SEPs); b) modifications due to brain stem hypoxia (vestibular and auditory centres) or of the internal ear for the early and middle auditory potentials (AEPs); c) modifications due to lower perfusion of the occipital lobes and of the nonspecific centres in the brain stem for the visual evoked potentials (VEPs). The N0-P0-Na component of the middle auditory response was considered to represent a vestibular response and it was significantly affected in cases with VBI and clinical manifestations like: equilibrium disorders, nystagmus and vertigo. Typical images of the sensory evoked responses affected by VBI are reproduced considering their evidence as an elective method in the paraclinical examination of this syndrome.
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PMID:Cerebral evoked potentials in the chronic vertebrobasilar insufficiency. 801 85

The territory of the lateral branch of the posterior inferior cerebellar artery (1PICA) supplies the anterolateral region of the caudal part of the cerebellar hemisphere. Because infarcts in the territory of the 1PICA have rarely been studied specifically, 10 patients with this type of infarct are reported. An 1PICA infarct was isolated in only three patients, whereas it was associated with brainstem infarct in four, with occipital infarct in one, and with multiple infarcts in two patients. The most common symptom at onset was acute unsteadiness and gait ataxia without rotatory vertigo (six patients). Unilateral cerebellar dysfunction was found in all patients, with limb ataxia (nine patients), dysdiadochokinesia (five patients), and ipsilateral body sway (four patients), but dysarthria and primary position nystagmus were notably absent. In the patients with a coexisting infarct in the brainstem, cranial nerve and sensorimotor dysfunction was prominent and often masked the signs of cerebellar dysfunction. Unlike other infarcts in the PICA territory, 1PICA territory infarcts were mainly associated with vertebral artery atherosclerosis (six patients), whereas cardiac embolism was less common (three patients). Unilateral limb ataxia without dysarthria or vestibular signs suggests isolated 1PICA territory infarction and should allow its differentiation from other cerebellar infarcts.
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PMID:Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery. 808 72

Of 2,130 consecutive patients admitted to two hospitals with acute brain infarction, we examined 11 patients (0.52%) with medial medullary infarction. The infarcts documented by MRI were unilateral in 9 patients and bilateral in 2 patients, and located in the anteromedial arterial territory of the upper or middle part of the medulla. Atherosclerosis of the vertebral arteries was the predominant vascular pathology. The vertebral artery was occluded at its terminal portion in 7 patients. Nine patients had hypertension, and 8 of these had additional risk factors. Male gender (10 patients) and smoking habits (7 patients) were more prevalent compared with patients with pontine infarction. One patient had a medial medullary infarction attributed to dissection of the vertebral arteries following blunt head injury. Limb weakness was the major symptom in all patients, and gaze-evoked nystagmus was also frequent (6 patients). Tongue weakness ipsilateral to the infarct, the classic sign of medial medullary syndrome, was evident in only 3 patients. The outcome was usually excellent.
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PMID:Medial medullary infarction: analyses of eleven patients. 890 19

To examine the influence of hyperlipidemia and smoking on age-related changes in caloric response and pure-tone hearing, a caloric test and pure-tone audiometry were performed in 14 healthy volunteers and in 78 tinnitus patients without subjective hearing loss. The patients were from 24 to 84 years of age, and were divided into 4 groups: the no-risk group (N group), the smoking alone group (S group), the hyperlipidemia alone group (L group), and the smoking plus hyperlipidemia group (S-L group). Slow phase eye velocity of the caloric nystagmus (SPEV) and average hearing level at high frequencies were compared between the N groups and the other groups. There was a significant difference in SPEV only between the N and S-L groups, but not in the hearing level. This suggests that age-related changes in the caloric response be promoted by atherosclerosis, unlike presbycusis.
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PMID:Influence of hyperlipidemia and smoking on age-related changes in caloric response and pure-tone hearing. 965 10

We report a case of a 42-year old man with a bilateral medial medullary stroke (MMS) with favorable outcome. First described by Spiller in 1908, the MMS accounts for less than 0,5% of all cerebral infarcts. It may be unilateral or more rarely bilateral, and may often be the consequence of the atherosclerosis. The clinical features of MMS classically associate contralateral hemiparesis and lemniscal hypoesthesia accompanied by ipsilateral lingual palsy and sometimes oculomotor disturbances (upbeat nystagmus). With the advent of magnetic resonance imaging, some restricted or unusual clinical manifestations can be attributed to this localization. The benign form of MMS seems much more common than MMS with poor prognosis.
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PMID:[Bilateral medial medullary infarction]. 1079 16

A 24-year-old female blue and gold macaw (Ara ararauna) was presented for an acute onset of left head tilt. On examination, the macaw was dehydrated and had a 120-degree left head tilt, decreased proprioception of the left pelvic limb, and intermittent vertical nystagmus. Results of hematologic testing and biochemical analysis revealed severe leukocytosis with lymphopenia and heterophilia and a high uric acid concentration. Radiographs showed bilateral intertarsal joint osteoarthritis and a healed ulnar fracture. Magnetic resonance imaging of the brain revealed focal T2 and fluid-attenuated inversion recovery hyperintense lesions in the right cerebral hemisphere and in the midbrain. The midbrain lesion showed susceptibility artifact on the T2* sequence, suggesting hemorrhage. In the T2* sequence, iron accumulation (as seen with hemorrhage) distorts the magnetic signal, resulting in the production of a susceptibility artifact, which can then be visualized as a region of hypointensity. The bird was hospitalized but died despite intensive care. Necropsy revealed multiple cerebral vascular lesions including an acute cerebral infarct, a ruptured midbrain aneurysm, and multifocal systemic atherosclerosis. To our knowledge, this is the first report of a cerebral aneurysm in a bird. This report correlates the clinical presentation, imaging, and histopathologic findings in a macaw with central vestibular disease and demonstrates how advanced imaging techniques can identify hemorrhagic lesions through the T2* sequence.
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PMID:Central vestibular disease in a blue and gold macaw (Ara ararauna) with cerebral infarction and hemorrhage. 2511 42