Disease relevance of Paresis

• Hemicrania with oculosympathetic paresis from isosorbide dinitrate [1].
• RESULTS: At the time of follow-up, 20 patients (31%) had no neurological deficits, 22 patients (34%) had minor deficits that did not interfere with their daily life activities, and 23 patients (35%) had moderate or severe deficits such as severe ataxia, spastic paresis, seriously reduced vision, or epilepsy with more than two seizures per year [2].
• In the other seven patients (one with weakness in the arms and legs, one with transient left hemiparesis, two with hearing loss, and three with various visual disturbances), chemotherapeutic agents (mainly cisplatin and vincristine) and underlying diseases probably contributed significantly to the occurrence of these complications [3].
• Its core elements are a suprabulbar paresis, a mild spastic tetraplegia and a significant excess of cognitive and behavioural impairments and epilepsy [4].
• Infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER [5].

Psychiatry related information on Paresis

• We report that members of a kindred affected by a slowly progressive dementia, seizures, ataxia, hemiparesis, and decreased vision without neuropathy have TTR amyloid deposits in the leptomeninges, the brain parenchyma, and the eye [6].
• Most had severe hemiparesis, mental retardation, porencephaly, and focal epilepsy [7].
• Neurological abnormalities comprised intellectual deterioration in 7, conduct disorder in five, dystonia in three, choreoathetosis in three, seizures in one and hemiparesis in one [8].
• The superficial cortex of the hemisphere contralateral to the hemiparesis and sensory neglect enhanced diffusely with gadolinium on T1-weighted MRI images [9].
• Complications were transient hemiparesis in two, transient hypernatraemia in 17, short-term memory impairment in 14 (persistent in four), weight gain in ten (persistent in five), need for supplemental thyroxine in five, and lowered growth hormone (uncertain clinical significance) in six [10].

High impact information on Paresis

• Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis [11].
• A combination of three tests with relatively high validity (paresis of abductor pollicis brevis muscle, hyperpathia, and flick sign) did not significantly change the probability of CTS [12].
• The rat zitter (zi) mutation induces hypomyelination and vacuolation in the central nervous system (CNS), which result in early-onset tremor and progressive flaccid paresis [13].
• Disease is manifested by ataxia, seizures, and paresis and leads to early death [14].
• The more marked the paresis of the elbow flexor and extensor muscles of the patients, relative to the strength of the normal subjects, the greater was this reduction in maximum velocity [15].

Chemical compound and disease context of Paresis

• In all patients anisotropy was reduced in the coronal radiata contralateral to the hemiparesis by more than 3 SD compared to control subjects [16].
• Oral treatment of rats with N-methyl-l -arginine acetate (l -NMA), beginning at peak disease on day 11 postimmunization, results in significant prolongation of disease and an alteration in the presentation of clinical symptoms from that of solely hind limb paresis/paralysis to severe fore limb involvement as well [17].
• One patient however, showing minor paresis of one leg, improved after institution of ganciclovir therapy 1 week after onset of symptoms [18].
• Therapy with acyclovir proved to be successful in animals showing paresis after infection even when the drug was given in lower than optimal dosages [19].
• We saw a patient with inactive SLE in whom hoarseness and exertional dyspnea developed as a result of arytenoiditis and vocal cord paresis during steroid tapering [20].

Biological context of Paresis

• Poliovirus type 1 was isolated from an immunodeficient patient 4 days after onset of paresis (IS1) and after 5.5 years of prolonged enteral virus replication (IS2) [21].
• We show that the overexpression of wild-type murine or human TNF-alpha transgenes by resident CNS astrocytes or neurons in sufficient to trigger a neurological disorder characterised by ataxia, seizures and paresis, with histopathological features of chronic CNS inflammation and white matter degeneration [22].
• Suxamethonium was shown to produce distinctive clinical features characterised by signs of both extraocular muscle contraction and paresis, manifest by symptoms of eye and eyelid heaviness without generalised paresis [23].
• Ocular alignment and saccades were studied in seven patients with trochlear nerve pareses, before and after strabismus surgery [24].
• The mutant strain of Wistar rats carrying an autosomal recessive gene defect is characterized by a sequence of progressively developing behavioural alterations including hyperexcitability, tremor, olfactory and gustatory automatisms, bradykinesia, ataxia, rigidity, paresis and cachexia [25].

Anatomical context of Paresis

• We describe a patient with isolated bilateral third nerve paresis, positive serological findings in blood and cerebrospinal fluid, CSF pheocytosis, and increased protein content [26].
• Deposition in the central nervous system leads to neurological dysfunction marked by dementia, spinal cord paresis, and cerebellar ataxia [27].
• Cocaine and pupillary-sparing oculomotor nerve paresis [28].
• Eight patients with unilateral phrenic nerve paresis, as indicated by a unilaterally elevated hemidiaphragm on a chest radiograph and maximum sniff PDI consistent with hemidiaphragm weakness, were all accurately identified by unilateral magnetic stimulation [29].
• However, motor paresis closely related to sympathetic dysfunction is quite a new condition that we call "sympathetic motor paresis." This is important clinically because a long-standing effect can be expected from permanent sympathetic ganglion block with dehydrated ethanol [30].

Gene context of Paresis

• Although IL-6 and sIL-6Ralpha single transgenic mice were free of neurological disease, IL-6/sIL-6Ralpha double-transgenic mice showed neurological signs, such as tremor, gait abnormalities, and paresis [31].
• RESULTS: Two unrelated patients with PBD without distinctive external features had normal neurodevelopmental milestones during their first year, followed by rapid deterioration including severe hypotonic pareses, seizures, retinopathy, and deafness [32].
• These results suggest that HGF/SF plays an important role in the development of gastrointestinal paresis and chronic intestinal inflammation [33].
• This paresis may account in part for the increased BMP-4 activity in fibrodysplasia ossificans progressiva [34].
• The presentation for AIS1 was hemiparesis in 77% and cerebellar symptoms and seizures in 20%, respectively [35].

Analytical, diagnostic and therapeutic context of Paresis

• At 16 h after ligation, marked decrements in uptake were observed in animals showing hemiparesis: Uptake values expressed as a percent of the corresponding control hemisphere were 15.2% for dopamine, 28.9% for GABA, and 47.5% for glutamate [36].
• A portable syringe pump was used to administer glucagon by intravenous infusion in order to achieve bowel paresis during abdominal computed tomography [37].
• Convulsions and temporary hemiparesis following spinal anesthesia in a child with moyamoya disease [38].
• Seizures, subdural effusions, and hemiparesis were found significantly more often during hospitalization in those with delayed sterilization of CSF [39].
• Administration of Decadron, chemotherapy and 3,000 rad cranial radiation resulted in dramatic improvement of dysphasia and right hand paresis [40].

References