Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six cases with CT scan evidence of paramedian thalamic lacunar infarcts in the region of the paramedian thalamic arteries (4 unilateral left and 2 bilateral) are described. The main acute symptoms included disorders of consciousness, hypersomnia and sometimes vertical gaze paresis. An amnesic syndrome of variable degree and duration was observed in all cases, and in 1 of them was still present 2 years after the onset. In addition, we report a case of lateral thalamic infarction, which showed a predominantly aphasic (transcortical sensory type) clinical picture.
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PMID:Lacunar thalamic infarcts and amnesia. 261 24

Five patients were examined suffering from bilateral paramedian thalamic infarction, caused by occlusion of the posterior paramedian thalamo-subthalamic arteries, when they begin from one single pedicle. All cases began with obnubilation or transitory coma, followed by hypersomnia. Four patients showed vertical gaze paralysis, and the fifth vertical nystagmus. In three cases, nuclear lesion of the III cranial nerve was observed along with alteration of the photomotor reflexes, and there was miosis in one case. All were suffering from weakness in one or another limb or facial paresis and generalised acute hypotonia: only one patient had hemihypostesia. All five had dysarthria, ataxy and dysmetria, one had asterixis and two spasmodic crying. Between 5 and 12 months later, one had akinetic mutism and vertical gaze paralysis as the most noteworthy signs. The neuroradiological images show a bilateral ischemic lesion in the paramedian thalamic region, which extends in some cases to the anterior nucleus and in one case to the pulvinars; the lesion continues through the subthalamic regions and the medial part of the mesencephalic tegmentum, with a clear extension to the medial region of the cerebral peduncles in three cases and to the tectum in one case.
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PMID:[Paramedian bithalamic infarct syndrome: report of five new cases]. 749 75

The paramedian thalamic arteries can arise as a pair from each P1 of the posterior cerebral artery, but they may also arise equally from a common trunk off one P1, thus supplying thalamus bilaterally. Such a common trunk is called the artery of Percheron and supplies the mesial aspects of both thalami and the rostral midbrain. This is a retrospective review of 1,253 consecutive patients with ischemic stroke enrolled in a stroke registry within an 8-year period (January 2001-December 2008). All were evaluated with detailed clinical and neuropsychological evaluation, magnetic resonance imaging (MRI), blood studies, electrocardiogram, and transthoracic echocardiography. All standard risk factors were recorded in these patients. Ten patients (0.7%) in this series presented with a first-ever thalamic stroke demonstrating bilateral paramedian thalamic lesions on MRI. The main cause of bilateral paramedian thalamic infarctions was small artery disease (60%), followed by cardioembolism (40%). A well-defined clinical picture is shown in bilateral paramedian thalamic artery infarcts. These patients had disorder's consisting of consciousness, memory dysfunctions, various types of vertical gaze paresis, and psychological changes. Although neurologic deficits and hypersomnia recovered to large extent in patients with paramedian thalamic infarcts, cognitive deficits that were mainly linked with bilateral and left-sided lesions often persisted. Vertical gaze paresis tended to improve and never seriously disturbed the patient's activities. We believe that these kinds of strokes have been commonly overlooked, especially without widespread use of MRI.
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PMID:Bilateral paramedian thalamic artery infarcts: report of 10 cases. 2061 Jan 85

Many late-stage chronic Lyme disease clinical findings are neuropsychiatric. A total clinical assessment is critical in diagnosis, especially since controversy surrounds the reliability of laboratory testing. The clinical findings of one hundred Lyme disease patients with chronic neuropsychiatric symptoms were entered into a database. The prevalence of each clinical finding pre-infection and post-infection was compared and calculated within the 95% confidence interval. Patients had minimal symptoms pre-infection, but a high post-infection prevalence of a broad spectrum of acquired multisystem symptoms. These findings included impairments of attention span, memory, processing, executive functioning, emotional functioning, behavior, psychiatric syndromes, vegetative functioning, neurological, musculoskeletal, cardiovascular, upper respiratory, dental, pulmonary, gastrointestinal, genitourinary, and other symptoms. The most prevalent symptoms included sustained attention impairments, brain fog, unfocused concentration, joint symptoms, distraction by frustration, depression, working memory impairments, decreased school/job performance, recent memory impairments, difficulty prioritizing multiple tasks, fatigue, non-restorative sleep, multitasking difficulties, sudden mood swings, hypersomnia, mental apathy, decreased social functioning, insomnia, tingling, word finding difficulties, name retrieval, headaches, sound hypersensitivity, paresis, anhedonia, depersonalization, cold intolerance, body temperature fluctuations, light sensitivity and dysfluent speech. The average patient had five symptoms pre-infection and 82 post-infection. Pattern recognition is critical in making a diagnosis. This study was used to develop three clinical assessment forms.
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PMID:A Clinical Diagnostic System for Late-Stage Neuropsychiatric Lyme Borreliosis Based upon an Analysis of 100 Patients. 3193 5