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Biomedical subjects

N Hermanowicz

Publications and source records attributed to N Hermanowicz.

10 recordsLinked to original sources
PubMed2001

Management of Parkinson's disease. Strategies, pitfalls, and future directions.

In coming years Parkinson's disease will become increasingly prevalent as the baby boom generation grows older. Diagnosis often is complicated and requires careful consideration of symptoms and neurologic findings. Optimal symptomatic treatment of Parkinson's disease involves an individualized approach with each patient and ongoing evaluation of benefits versus side effects. Neurosurgical intervention is an option for some patients who are not adequately helped by medical therapy. New treatments (e.g., stem cell therapy) are currently being studied and may be available in the foreseeable future.

Antiparkinson Agents↗
PubMed1998

Temporal processing in the basal ganglia.

This study investigated the role of the basal ganglia in timing operations. Nondemented, medicated Parkinson's disease (PD) patients and controls were tested on 2 motor-timing tasks (paced finger tapping at a 300- or 600-ms target interval), 2 time perception tasks (duration perception wherein the interval between the standard tone pair was 300 or 600 ms), and 2 tasks that controlled for the auditory processing (frequency perception) demands of the time perception task and the movement rate (rapid tapping) in the motor-timing task. Using A.M. Wing and A.B. Kristofferson's (1973) model, the total variability in motor timing was partitioned into a clock component, which reflects central timekeeping operations, and a motor delay component, which estimates random variability due to response implementation processes. The PD group was impaired at both target intervals of the time perception and motor-timing tasks. Impaired motor timing was due to elevated clock but not motor delay variability. The findings implicate the basal ganglia and its thalamocortical connections in timing operations.

Aged↗
PubMed1997

Cognitive-motor learning in Parkinson's disease.

Procedural learning deficits are common in Parkinson's disease (PD), but contradictory results have been reported in rotary pursuit learning. This article compared rotary pursuit learning in 2 nondemented PD groups and 2 normal control (NC) groups, using a between-subjects group design in which 3 rotation speeds were presented either randomly or in blocks. The pattern of learning differed between the randomized and the blocked conditions in the NC, but not in the PD groups. Learning was impaired in the PD group in the random condition only. Memory, visuospatial, or executive skills were not associated with the PD group's poorer learning in the randomized context. Results show that procedural learning deficits are not universal with basal ganglia abnormalities but rather depend on the specific cognitive requirements of the learning context.

Aged↗
PubMed1991

Posttraumatic torticollis.

We report six cases of torticollis precipitated by neck trauma. The dystonia began 1 to 4 days after the trauma and differed clinically from idiopathic torticollis by marked limitation of range of motion, lack of improvement after sleep ("honeymoon period"), and absence of geste antagonistique. Worsening with action was not present; nor was there improvement with support as seen with idiopathic torticollis. Onset of pain immediately after the trauma and marked spasms of the paracervical muscles were other predominant features. Anticholinergic therapy was without benefit; however, some improvement occurred with botulinum toxin injection. It is concluded that torticollis can be caused by peripheral trauma and that it has unique clinical characteristics.

Adult↗
PubMed1991

Treatment of oromandibular dystonia with botulinum toxin.

Botulinum toxin produces muscle weakness by inhibition of acetylcholine release at the neuromuscular junction. The toxin has been used successfully for symptomatic treatment of focal dystonias. Our experience in the use of botulinum toxin for the treatment of oromandibular dystonia in five patients is reported. Improvement following treatment was reported as marked by 1 patient, moderate by 1 patient, and mild by 3 patients. Similar improvement was noted by the examiners. One patient with mild cosmetic improvement developed significant dysphagia requiring feeding by a nasogastric tube for a 3-month period.

Botulinum Toxins↗
PubMed1984

Abnormal membrane protein methylation and merocyanine 540 fluorescence in sickle erythrocyte membranes.

Sickle cell erythrocytes exhibit reduced carboxyl methylation of membrane proteins compared to normal erythrocytes. This altered methylation in sickle membrane proteins is also observable when extracted membranes, both intact and alkali treated, were used as substrates for the homologous protein methylase II (S-adenosylmethionine:protein-carboxyl O-methyltransferase, EC. 2.1.1.24). However, when glycophorin A, one of the major methyl acceptors in both membranes, was extracted by lithium diiodosalicylate and used as the methyl acceptor, the proteins from both membranes were methylated equally, suggesting an involvement of membrane structure in membrane-bound protein methylation. Merocyanine 540 (MC-540), a fluorescent probe, was used to determine if the membranes differed in organization. Incubation of both normal and sickle erythrocytes membranes with MC-540 produced a marked increase in extrinsic fluorescence, reflecting a relatively nonpolar environment for the dye bound to the membranes. The fluorescence from sickle cell ghosts was only 87% as intense as that from normal ghosts, while the actual amount of MC-540 associated with sickle cell membranes was only 62% of normal. These data suggest that differences exist in the distribution of surface charges on these plasma membranes. These results are consistent with the hypothesis that abnormal levels of membrane protein methylation observed in sickle erythrocytes may be a result of abnormal membrane organization characteristic to sickle cell anemia.

Anemia, Sickle Cell↗
PubMed1982

Involvement of spectrin in the maintenance of phase-state asymmetry in the erythrocyte membrane.

The fluorescent probe merocyanine 540 does not stain the plasma membrane of normal human or murine erythrocytes, nor of genetically abnormal human spherocytic erythrocytes. It does, however, stain erythrocyte membranes in several systems in which the underlying spectrin network is altered or missing. Because of the greater affinity of merocyanine 540 for fluid--phase lipid bilayers, these results suggest that the external leaflet of erythrocyte membranes becomes more disordered upon alteration or loss of the internal spectrin network. Analysis of the transbilayer arrangement of membrane phospholipids by digestion with phospholipase A2 suggests that lipid compositional asymmetry of the erythrocyte membrane is responsible for a phase-state asymmetry between the two lipid leaflets, and that spectrin is required to maintain this asymmetry and the gel-like state of the external leaflet.

Animals↗