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Biomedical subjects

B R Bloem

Publications and source records attributed to B R Bloem.

At least 19 recordsLinked to original sources
PubMed1999

Are automatic postural responses in patients with Parkinson's disease abnormal due to their stooped posture?

Abnormal automatic postural responses are thought to contribute to balance impairment in Parkinson's disease. However, because postural responses are modifiable by stance, we have speculated that some postural abnormalities in patients with Parkinson's disease are secondary to their stooped stance. We have studied this assumption by assessing automatic postural responses in 30 healthy subjects who were instructed either to stand upright or to assume a typical parkinsonian posture. During both conditions, subjects received 20 serial 4 degrees 'toe-up' rotational perturbations from a supporting forceplate. We recorded short-latency (SL) and medium-latency (ML) responses from stretched gastrocnemius muscles and long-latency (LL) responses from shortened tibialis anterior muscles. We also assessed changes in the center of foot pressure (CFP) and the center of gravity (COG). The results were qualitatively compared to a previously described group of patients with Parkinson's disease who, under these circumstances, typically have large ML responses, small LL responses and insufficient voluntary postural corrections, accompanied by a slow rate of backward CFP displacement and an increased posterior COG displacement. The stooped posture resulted in unloading of medial gastrocnemius muscles and loading of tibialis anterior muscles. Onset latencies of stretch responses in gastrocnemius muscles were delayed in stooped subjects, but the onset of LL responses was markedly reduced. Amplitudes of both ML and LL responses were reduced in stooped subjects. Prestimulus COG and, to a lesser extent, CFP were shifted forwards in stooped subjects. Posterior COG displacement and the rate of backward CFP displacement were diminished in stooped subjects. Voluntary postural corrections were unchanged while standing stooped. These results indicate that some postural abnormalities of patients with Parkinson's disease (most notably the reduced LL responses) can be reproduced in healthy subjects mimicking a stooped parkinsonian posture. Other postural abnormalities (most notably the increased ML responses and insufficient voluntary responses) did not appear in stooped controls and may contribute to balance impairment in Parkinson's disease.

Adult↗
PubMed1998

[Don't let the patient with Parkinson's disease fall!].

Three patients with a hypokinetic-rigid syndrome, a woman aged 69 years and two men aged 62 and 67 years, were admitted because of frequent falling. In two patients Parkinson's disease was diagnosed, the third had progressive supranuclear palsy. Balance impairment and falls typically emerge late in the course of Parkinson's disease. Falls can have dramatic physical consequences, such as (hip) fractures, and often induce a fear of additional falls which further impairs mobility and social contacts. The pathophysiology of falls in Parkinson's disease is complex and appears to result from both impaired balance regulation and commonly occurring balance disturbances (due to the shuffling gait and dyskinesias). Balance impairment often responds insufficiently to pharmacological treatment. Aspecific measures such as physical therapy, walking aids and reduction of domestic hazards can reduce the number of falls. Because patients often fail to voluntarily report their falls, physicians must actively pay attention to balance impairment in Parkinson's disease.

Accidental Falls↗
PubMed1998

Clinimetrics of postural instability in Parkinson's disease.

Judgement of the ability to recover balance after a sudden shoulder pull is used as a clinical measure of postural instability in Parkinson's disease. To further evaluate its merits, we compared this 'retropulsion test' with dynamic posturography in 23 Parkinson patients. Dynamic posturography involved 20 serial 'toe-up' support surface rotations, which induced backward body sway. We found a moderate correlation (Spearman's p = 0.54; P < 0.05) between the retropulsion test and body sway after platform rotations during the 'off' phase, but no correlation during the 'on' phase (Spearman's p = 0.43; P = 0.11). These results cast doubt on the use of the retropulsion test as a measure of postural instability in Parkinson's disease.

Adult↗
PubMed1998

Postural reflexes in patients with HIV-1 infection.

OBJECTIVE: We studied whether medium latency (ML) and long latency (LL) postural reflexes, which are abnormal in a number of neurological conditions including basal ganglia disorders, provide an early marker of CNS involvement in HIV-positive patients. METHODS: Leg reflexes were elicited in 9 neurologically normal HIV-positive patients and 10 healthy controls who were standing upright, using toe-up forceplate rotations of varying amplitude (4 degrees and 10 degrees) and predictability (serial and random). RESULTS: For predictable amplitude perturbations, posturally destabilizing ML and stabilizing LL responses in HIV-seropositives did not differ from controls. However, for unpredictable amplitude perturbations, HIV-positive patients inappropriately manifested a mid-size default LL response, in contrast to healthy subjects who showed a maximum size default response. CONCLUSIONS: These results suggest that impaired modulation of LL reflex processing occurs in early stages of HIV infection, prior to the onset of clinical postural instability, and this dysregulation may be influenced by cognitive factors.

Adult↗
PubMed1998

Prolonged coma and severely attenuated EEG after a single seizure.

A 63-year-old woman presented with a comatose state after a fall. Results of cranial computed tomography (CT) and magnetic resonance imaging (MRI) scans were normal. An EEG recorded 5 h after admission was very severely attenuated and slowed. Consciousness and EEG were improved the next day. No cause was detected initially. After sleep deprivation, the patient had a generalized seizure followed by a similar coma and EEG. Even a single seizure may cause a prolonged coma with a very severely attenuated and slowed EEG.

Accidental Falls↗
PubMed1997

Prolonged duration of standing up is an early dopa-sensitive abnormality in Parkinson's disease.

We studied the influence of dopaminergic medication on the duration of standing up, static posture and gait in five patients with Parkinson's disease (Hoehn and Yahr stage 1.5 to 3) and four healthy controls, using an optoelectronic camera system. Duration of standing up was prolonged in patients, while static posture and gait were largely unaffected. The prolonged duration of standing up was corrected by dopaminergic medication. These results suggest that an increased duration of standing up is a relatively early and dopa-sensitive abnormality in Parkinson's disease.

Aged↗
PubMed1997

[Gait impairment in the oldest old].

To evaluate senile gait patterns in octogenarians and nonagenarians, we provided a standardized questionnaire on gait disabilities to 153 elderly subjects over 88 years of age. Subjects represented a relatively healthy subgroup of non-institutionalized residents who participated in a gerontological survey of all inhabitants of the city of Leiden who were 85 years or older. Of the 142 subjects who responded to this questionnaire, 87 persons (61%) claimed distinct diseases as a cause of gait impairment. Of the remaining 55 persons, 42 received a standardized gait assessment. Gait was classified as completely normal in 25 persons (18% of all responders), whereas in three other persons gait could not reliably be classified as either normal or abnormal. A wide spectrum of clear gait abnormalities-mainly with ataxic features-was encountered in the remaining 14 persons (10%). It is concluded that some elderly subjects have a mainly ataxic gait disturbance which seems unrelated to the presence of distinct diseases. Although additional investigations might still reveal underlying pathology in these subjects, their gait impairment may represent the "idiopathic senile gait disorder'. In addition, a relatively high number of very old community residents have a completely normal gait.

Aged↗
PubMed1996

Influence of dopaminergic medication on automatic postural responses and balance impairment in Parkinson's disease.

It is still unclear why balance impairment in Parkinson's disease (PD) often responds insufficiently to dopaminergic medication. We have studied this issue in 23 patients with idiopathic PD and 24 healthy controls. Our specific purposes were (a) to investigate the contribution of abnormal automatic postural responses to balance impairment in PD and (b) to assess the influence of dopaminergic medication on abnormal automatic postural responses and balance impairment. Standing subjects received 4 degrees "toe-up" rotational perturbations of a supporting forceplate. We bilaterally recorded posturally destabilizing medium latency (ML) responses from the stretched gastrocnemius muscles and functionally corrective long latency (LL) responses from the shortened tibialis anterior (TA) muscles. We also assessed changes in the center of foot pressure (CFP) and the center of gravity (COG). All patients were tested in the "off" and "on" phases. All controls were tested and retested after 1 h. During the off phase, we found enlarged ML amplitudes and diminished LL amplitudes in patients, together with a markedly increased posterior displacement of the COG. The abnormal ML and LL responses were partially responsible for the increased body sway in patients because the initial forward (destabilizing) displacement of the CFP was increased, while the subsequent backward displacement of the CFP (a measure of the corrective braking action of LL responses) was delayed. Abnormal late automatic or possibly more voluntary postural corrections also contributed substantially to the increased body sway. During the on phase, ML amplitudes were reduced in patients but remained increased compared with controls. LL amplitudes no longer differed between both groups due to a modest, possibly dopamine-related increase in patients and a simultaneous decrease in controls. The abnormal CFP displacement was only partially improved by dopaminergic medication. The later postural corrections were not improved at all. Consequently, the increased posterior COG displacement was not ameliorated during the on phase. We conclude that (a) a combination of abnormal automatic and perhaps more voluntary postural corrections contributes to increased body sway in PD and (b) dopaminergic medication fails to improve balance impairment in PD because early automatic postural responses are only partially corrected, while later occurring postural corrections are not improved at all. These electrophysiological results support clinical observations and suggest that nondopaminergic lesions play a significant role in the pathophysiology of postural abnormalities in PD.

Adult↗
PubMed1995

Long latency postural reflexes are under supraspinal dopaminergic control.

Scaling of posturally stabilizing long latency (LL) reflexes in tibialis anterior muscles induced by "toe-up" rotational perturbations is abnormal in standing patients with Parkinson's disease. To investigate the contribution of dopaminergic pathways to abnormal scaling, we studied LL reflexes in 22 patients with selective hypodopaminergic syndromes: 10 psychiatric patients taking chronic neuroleptic medication (7 with mild parkinsonism), 8 patients with young-onset Parkinson's disease, and 4 patients with MPTP-induced parkinsonism. Results were compared with those of 10 healthy controls. Stimuli consisted of (a) 10 serial (predictable) perturbations of 4 degrees amplitude, (b) 10 serial (predictable) perturbations of 10 degrees amplitude, and (c) 20 randomly mixed (unpredictable) perturbations of either 4 or 10 degrees amplitude. In normal subjects, LL reflex amplitudes were adapted to match predictable variations in stimulus size, whereas under unpredictable conditions a "default" response emerged that anticipated the 10 degrees perturbation. LL reflex scaling under predictable conditions was intact in patients with neuroleptic-induced parkinsonism and young-onset Parkinson's disease, but the large default LL response under unpredictable conditions was absent. In patients with MPTP-induced parkinsonism, LL reflex scaling was absent during both predictable and unpredictable conditions. We conclude that abnormal scaling of posturally stabilizing LL reflexes is related to decreased supraspinal dopaminergic influence.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Postural reflexes in Parkinson's disease during 'resist' and 'yield' tasks.

Postural reflexes in leg muscles appear to be set at a fixed gain in Parkinson's disease. To further investigate gain adaptation, we instructed 16 patients with idiopathic Parkinson's disease (studied during the 'off' phase) and 21 healthy controls to either 'resist' or 'yield' in response to 20 serial 4 degrees toe-up perturbations of a supporting platform on which they were standing. We bilaterally recorded destabilizing medium latency (ML) reflexes from stretched gastrocnemius muscles and corrective long latency (LL) reflexes from shortened tibialis anterior muscles. We also assessed changes in center of foot pressure (CFP) and center of gravity (COG). During the 'resist' condition, patients had increased destabilizing ML reflexes, decreased corrective LL reflexes, increased backward displacement of the COG and increased forward (destabilizing) displacement of the CFP. In addition, the backward (corrective) displacement of CFP between 150 and 250 ms was delayed. During the 'yield' condition, reflex gains were modified in controls: LL reflexes were markedly attenuated, whereas ML reflexes were markedly increased. Although this reflex pattern resembled the 'resist' condition in patients, it was not associated with an increased forward displacement of the CFP, but only with a strongly delayed backward displacement of CFP which started after 150 ms. In patients, ML reflex amplitudes remained unchanged during the 'yield' condition, suggesting a fixed reflex gain. LL reflex amplitudes were reduced in patients but significantly less compared to controls, which again suggests a fixed reflex gain. This 'inflexibility' of postural reflexes was reflected by the CFP which showed much smaller changes between 0 and 250 ms in patients than controls. These results could not be ascribed to a different ability to yield because posterior displacement of the COG was identical in patients and controls during the 'yield' condition. We conclude that (1) patients with Parkinson's disease have abnormal and 'inflexible' postural reflexes, associated with delayed corrective movements about the ankle joint and increased body sway; and (2) the increased forward displacement of the CFP in patients likely reflects high stiffness in ankle muscles because reflex changes in controls only affected the CFP more than 150 ms after the perturbation. The increased muscle stiffness and inflexibility of postural reflexes in Parkinson's disease may contribute to balance impairment in daily life.

Adaptation, Physiological↗
PubMed1995

Clinical correlates of motor performance during paced postural tasks in Parkinson's disease.

Bradykinesia and hypokinesia may both play a significant role in postural instability commonly seen in patients with Parkinson's disease. We investigated which factor--movement time or movement amplitude--is the more significant limiting variable in patients with Parkinson's disease during a paced postural task. We also assessed the effect of antiparkinson medication upon these movement factors and the degree of correlation with changes in clinical performance. Subjects performed paced left-right (L-R) and forward-backward (F-B) continuous weight-shifting tasks at slow, medium and fast paces. Ten Parkinson patients were studied both OFF and ON their usual antiparkinson medication. Ten age-matched healthy controls were also tested and subsequently retested on the same schedule as the patients. Movement times and amplitudes were measured and correlated with clinical changes in UPDRS motor subscores. Parkinson patients performed similar to controls with respect to movement time, but significantly displayed underscaled (reduced) movement amplitude. Movement amplitude improved after antiparkinson medication, but remained significantly less than that of controls. Improvements in L-R movement amplitude correlated with clinical improvements in bradykinesia and postural instability, while improved F-B movement amplitude correlated only with reduced postural instability. We conclude that hypometric movement amplitude, and not abnormal movement time, is the primary abnormality observed in Parkinson patients during a paced postural task. Amplitude underscaling seems antiparkinson medication-dependent and improvement correlates with favorable clinical changes in bradykinesia and postural instability scores.

Aged↗
PubMed1994

Medium latency stretch reflexes in young-onset Parkinson's disease and MPTP-induced parkinsonism.

It is still unclear why components of the phasic stretch reflex are increased in Parkinson's disease (PD). To study the role of aging, we assessed medium latency (ML) stretch reflexes in 19 Parkinson patients (8 with young-onset PD, 11 with late-onset PD) and 23 normal subjects (10 young, 13 old). To assess the contribution of supraspinal dopaminergic influences, we also studied 5 young parkinsonian patients with a selective central dopamine deficiency induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). ML responses were recorded from the medial gastrocnemius muscle which was stretched by 4 degrees toe-up rotations of a platform upon which subjects were standing. ML responses were significantly enhanced in late-onset patients compared with older controls. In contrast, ML responses did not differ between young-onset patients and young controls. This observation could be attributed to the significantly different influence of age on ML-amplitudes in patients and controls. Thus, ML-amplitudes declined with age in controls, whereas they increased with age in PD possibly because older patients were more severely affected than younger patients. Thus, the difference between young-onset and late-onset PD seems to be related to the opposite effects of increasing age and disease severity in patients and controls. ML-amplitudes did not differ between patients with MPTP-induced parkinsonism, patients with young-onset PD and controls, suggesting that supraspinal dopaminergic systems are not critically involved in control of ML responses. This result also indicates that the severity effect in PD may be related to disruption of non-dopaminergic pathways which occurs in late-onset, but not young-onset patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗