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Biomedical subjects

C G Goetz

Publications and source records attributed to C G Goetz.

At least 199 records · Page 11Linked to original sources
PubMed1988

Relationship of aluminum to neurocognitive dysfunction in chronic dialysis patients.

Aluminum has been proposed as the causative agent in dialysis encephalopathy syndrome. We prospectively assessed whether other, less severe, neuropsychologic abnormalities were also associated with aluminum. A total of 16 patients receiving chronic dialytic therapy were studied. The deferoxamine infusion test (DIT) was used to assess total body aluminum burden. Neurologic function was evaluated by quantitative measures of asterixis, myoclonus, motor strength, and sensation. Cognitive function was assessed by measures of dementia, memory, language, and depression. There were four patients with a positive DIT (greater than 125 micrograms/L increment in serum aluminum) that was associated with an increase in the number of neurologic abnormalities observed, as well as an increase in severity of myoclonus, asterixis, and lower extremity weakness. Patients with a positive DIT also showed significant impairment in memory; however, no differences were noted on tests of dementia, depression, or language. There was no significant correlation between sex, age, presence of diabetes, mode of dialysis, years of chronic renal failure, years of dialysis or years of aluminum ingestion and any neurologic or neurobehavioral measurement, serum aluminum level, or DIT. These changes may represent early aluminum-associated neurologic dysfunction.

Adult↗
PubMed1987

Clonidine and Gilles de la Tourette's syndrome: double-blind study using objective rating methods.

Clonidine has been suggested to be effective in Gilles de la Tourette's syndrome (GTS), but no double-blind study has ever evaluated its effects using objective measures. Thirty patients with GTS completed a 6-month placebo-controlled crossover study of the effectiveness of clonidine. Videotapes were obtained at each 3-week visit and were evaluated randomly at the end of the study for distribution, frequency, and severity of motor and vocal tics. Quantifiable psychometric examinations were performed as well. The use of clonidine did not significantly (p less than 0.05) reduce motor tics, vocalizations, or behavior. The effect of a low dose (0.0075 mg/kg/day) was no different from that of a high dose (0.015 mg/kg/day); children's responses were no different from adults'; and those also receiving neuroleptic agents showed the same lack of efficacy as seen in patients on no other medication. Dosing schedule did not affect the objective ratings; scores from clonidine given twice a day were equivalent to those for three times a day.

Adolescent↗
PubMed1987

The autonomic nervous system in Gilles de la Tourette's syndrome.

Twenty-three patients with Gilles de la Tourette's syndrome (GTS) underwent noninvasive investigation of autonomic nervous system (ANS) function, as did 23 age-matched controls. ANS function in GTS patients was no different from that of controls, and patients receiving neuroleptic drugs had the same ANS function as untreated patients. All 23 patients later received clonidine and were retested. The ANS values before administration of clonidine were compared with those while patients were taking clonidine. The only significant change (p less than 0.01) with clonidine was a reduced resting pulse rate. The combination of clonidine and neuroleptic drugs did not induce significant autonomic changes compared with neuroleptic therapy alone. These results indicate that the ANS in GTS patients is normal and that the drugs used to abate tics do not produce clinically significant changes in ANS when chronically given. The findings suggest that the pathophysiology and treatment of GTS do not directly involve the nuclei or tracts of autonomic regulation.

Adolescent↗
PubMed1987

Amantadine and motor fluctuations in chronic Parkinson's disease.

Twenty patients with idiopathic Parkinson's disease (PD) and motor fluctuations received open-label amantadine (100-200 mg/d) in addition to their other antiparkinson medications. One patient had unpredictable motor fluctuations (on-off) and the others had end-of-dose wearing-off. The effect of amantadine on motor fluctuations and parkinsonian disability was tested at 1, 2, and 3 months. Moderate improvement in motor fluctuations occurred in 55% of the patients at 2 months and 65% of patients at 3 months of treatment (p less than 0.01). There was also significant improvement in parkinsonian disability. The duration of improvement averaged 5.7 months, and all patients deteriorated to their baseline level of function within 12 months. This study suggests that the addition of amantadine can transiently improve motor fluctuations and have a significant impact on overall disability in patients with chronic PD.

Adult↗
PubMed1987

Progression of Parkinson's disease without levodopa.

We studied 100 consecutive patients with Parkinson's disease (PD) who were not receiving levodopa and followed them until symptoms advanced and levodopa was given. Eighty-three patients eventually received levodopa; 50% started within 36 months after a mean duration of symptoms of 48 months. Patients starting on levodopa showed significant progression of their disease compared with their baseline examination. These data have direct applicability to the design and implementation of future protocols aimed at preventing disease progression of PD.

Humans↗
PubMed1987

Parkinson's disease and motor fluctuations: long-acting carbidopa/levodopa (CR-4-Sinemet).

Long-acting levodopa/carbidopa combination (CR-4-Sinemet) was compared with traditional levodopa/carbidopa (Sinemet) open label in 20 patients with Parkinson's disease and "wearing-off" phenomena. After 4 to 6 weeks of therapy with CR-4-Sinemet, the number of daily doses of medication dropped significantly compared with traditional Sinemet, disability improved, and "on" time increased. In nine patients receiving CR-4-Sinemet for 3 months, the number of daily doses and the on time without chorea remained significantly improved. CR-4-Sinemet peaked in plasma after 2 hours, and moderately high levels remained at 4 hours after the dose. Side effects were similar between traditional Sinemet and CR-4 Sinemet.

Adult↗
PubMed1987

Charcot at the Salpêtrière: ambulatory automatisms.

Jean-Martin Charcot, as professor of neurology at the Salpêtrière Hospital in Paris, delivered a series of dialogue case presentations on general neurology in 1887-1889. These cases, never before translated into English, provide a first-hand view of Charcot's renowned teaching method and his opinions on many neurologic topics. One patient with bizarre ambulatory spells probably representing absence status was recognized by Charcot as an epileptic. This otherwise healthy young man, without a history of generalized epilepsy or hysteria, experienced multiple spells during which he suddenly became unaware of his surroundings, rambled throughout Paris and its outskirts, and had complex interactions with other people. As Charcot unraveled the diagnostic mystery, he traced the patient's wanderings and analyzed the differential diagnosis, treatment, and pathophysiology of these intermittent spells.

Adult↗
PubMed1987

A rating scale for Gilles de la Tourette's syndrome: description, reliability, and validity data.

We developed a rating scale for tic disorders that uses only objective criteria and accommodates the variety of tic manifestations. Using short videotaped recordings with the examiner out of the taping room, we measured five tic variables: number of body areas affected, frequency of motor tics and vocalizations, and severity of motor tics and vocalizations. The rating scale fulfilled tests for inter-rater reliability and temporal stability, and correlated well with scales used to assess global changes over prolonged periods. It objectively detected improvement in tics with neuroleptics, the one pharmacotherapy accepted to abate tics in most patients.

Clonidine↗
PubMed1986

The effect of thioridazine on haloperidol induced behavioral hypersensitivity.

Behavioral Hypersensitivity (BH) to dopamine agonists occurs following chronic treatment with most neuroleptics including haloperidol. In the present study we observed that the concurrent administration of thioridazine and haloperidol prevented the development of BH. In contrast, another neuroleptic, fluphenazine, coadministered with haloperidol, potentiated the degree of BH relative to animals treated with haloperidol only. In rats already made hypersensitive by chronic treatment with haloperidol, a 4 week subsequent treatment with normal saline, thioridazine alone of thioridazine in combination with haloperidol, produced normal behavioral responsiveness. These results suggest that thioridazine prevents the development of BH and can reverse the expression of haloperidol-induced BH.

Animals↗
PubMed1986

The effect of antimuscarinic agents on haloperidol induced behavioral hypersensitivity.

Varying doses of scopolamine, trihexyphenidyl and benztropine were administered to rats or guinea-pigs by themselves or in combination with 0.5 mg/kg haloperidol for 24 days. All animals were then challenged with 0.75 mg/kg apomorphine and assessed for stereotypic behavior following a 96 h drug free interval. Animals treated with haloperidol alone exhibited behavioral hypersensitivity to apomorphine challenge. Animals treated with both an antimuscarinic agent and haloperidol exhibited a significant reduction in behavioral responsiveness relative to animals treated with only haloperidol. This reduction was directly proportional to the antimuscarinic dose administered. A non-significant trend toward hyposensitivity was observed in animals who had been treated with antimuscarinic agents alone. These results suggest that the development of behavioral hypersensitivity may reflect CNS alterations in cholinergic as well as dopaminergic activity.

Animals↗
PubMed1986

Charcot on Parkinson's disease.

Charcot saluted Parkinson for his early observations, but condemned his use of the term "paralysis agitans." He emphasized that patients were neither dramatically weak nor were they necessarily plagued with tremor. Charcot suggested the name "Parkinson's disease," although he could not resist the comment in his amphitheater lecture series at the Salpêtrière that French physicians (unnamed) had probably described the disorder before 1817. Tremor, rigidity, postural instability, and bradykinesia were all recognized by Charcot. He classified the disorder as a "névrose," meaning a neurologic disorder without a known pathologic lesion, and found little benefit from therapies available at the time, including belladonna and ergot products.

France↗