Akinesia in Parkinson's disease

Schwab, Robert S.; England, Albert C.; Peterson, Elizabeth

doi:10.1212/wnl.9.1.65

Cited by 150 publications

(83 citation statements)

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“…We did not find signs of Parkinson's disease or other extrapyramidal disorders in our patients. Moreover, in parkinsonians, freezing gait usually appears late in the course of the disease, is often affected by levodopa therapy, and often coexists with tremor, rigidity, and bradykinesia (13)(14)(15). The total lack of response to levodopa in our patients supports distinction of PPFG from Parkinson's disease and suggests that freezing was probably not due to loss of nigral neurons.…”

Section: Discussionsupporting

confidence: 55%

Primary progressive freezing gait

et al. 1993

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Freezing gait is an incapacitating symptom often observed in patients with Parkinson's disease. It has been less frequently described in association with multi-infarct state, multisystem atrophies, and normotensive hydrocephalus. In our movement disorder clinic, we have diagnosed (and followed up to 3 years; median, 16 months), 18 patients in whom progressive freezing gait was the sole neurological dysfunction. These 15 men and 3 women (aged 60-82 years; 74 +/- 6) were subjected to an extensive neurological workup that included clinical evaluation, videotaping for grading of gait disability, comprehensive blood and cerebrospinal fluid (CSF) analysis, and brain computed tomography (CT) and magnetic resonance imaging (MRI). Mean disease duration was 2.5 +/- 1.9 years (range, 0.5-6). Neurological examination disclosed freezing gait, often associated with varying degrees of postural instability. The degree of freezing gait ranged from sudden motor blocks only when confronted with obstacles to severe disability with total inability to start walking requiring a walker, massive assistance, or a wheelchair. However, patients could mimic gait movements with absolutely no freezing when seated or lying prone, and most of them could overcome arrests by the "walking-over-lines" maneuver. Otherwise, neurological examination was normal with no signs of bradykinesia, rigidity, or tremor. Blood chemistry and CSF analysis were normal. Brain CT and MRI were normal or showed mild cortical atrophy in 12 and putative lacunes in 6 patients. Therapy with levodopa or dopamine agonists was ineffective. During the follow-up period, a gradual progression of the freezing gait was observed. However, it remained unaccompanied by any other neurological findings.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 55%

Primary progressive freezing gait

et al. 1993

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“…The nature of bradykinesia reinforces this idea. As described above, PD patients can move faster when reminded to (Schwab et al 1959), and when they make faster movements, these are kinematically normal (Mazzoni et al 2007). Thus, bradykinesia may simply reflect a change in selection parameters, so that the speed that is selected as appropriate is lower than normal.…”

Section: Motor Symptoms Of Pd and Normal Function Of The Bgmentioning

confidence: 89%

“…PD does not cause weakness thus defined. This was clearly shown by Schwab et al (1959), who asked a PD patient to repeatedly squeeze a rubber bulb igure 1. Long-latency reflexes are larger than normal in Parkinson's disease.…”

Section: Rigidity and Motor Controlmentioning

confidence: 94%

“…Such studies allow us to understand certain disorders, such as stroke, in terms of how much ability these disorders remove from normal motor function. However, PD does not impair strength (Fahn 2003), and patients can usually move faster, or apply more force, when reminded to do so (Schwab et al 1959). Instead, it is as if patients "select" abnormally slow movement speeds (Mazzoni et al 2007).…”

Section: Bradykinesia As Abnormal Speed Selectionmentioning

confidence: 99%

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Motor Control Abnormalities in Parkinson's Disease

Mazzoni

Shabbott²,

Cortes³

2012

Cold Spring Harbor Perspectives in Medicine

204

122

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The primary manifestations of Parkinson's disease are abnormalities of movement, including movement slowness, difficulties with gait and balance, and tremor. We know a considerable amount about the abnormalities of neuronal and muscle activity that correlate with these symptoms. Motor symptoms can also be described in terms of motor control, a level of description that explains how movement variables, such as a limb's position and speed, are controlled and coordinated. Understanding motor symptoms as motor control abnormalities means to identify how the disease disrupts normal control processes. In the case of Parkinson's disease, movement slowness, for example, would be explained by a disruption of the control processes that determine normal movement speed. Two long-term benefits of understanding the motor control basis of motor symptoms include the future design of neural prostheses to replace the function of damaged basal ganglia circuits, and the rational design of rehabilitation strategies. This type of understanding, however, remains limited, partly because of limitations in our knowledge of normal motor control. In this article, we review the concept of motor control and describe a few motor symptoms that illustrate the challenges in understanding such symptoms as motor control abnormalities.T he effects of Parkinson's disease (PD) can be described at different levels. Within the brain, the major pathological change is progressive degeneration of neurons in the pars compacta of the substantia nigra, one of the nuclei that constitute the basal ganglia (BG). These neurons normally transmit dopamine to another BG nucleus, the striatum, but their degeneration leads to dysfunction of these neuronal circuits that include the BG and motor cortical areas. At the level of an individual's behavior, these changes result in movement abnormalities, which are the major manifestations of the disease. These difficulties, in turn, cause major disruptions that range from an individual's quality of life to society-wide economics. Our goal in this article is to describe motor symptoms of PD at the level of motor control. We briefly review what is meant by "motor control" and describe the process of understanding a symptom as a motor control abnormality. We then focus on selected symptoms that, among the many and varied motor symptoms of PD, have been most studied from a motor control perspective.

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“…5 Kinematic studies have consistently shown that both movement time for single movements and inter-onset latency for sequential movements are increased. Although all types of movements are slower in PD, there is some evidence that externally triggered movements are less impaired than those that are self-initiated; this is best exemplifi ed by gait improvement when external cues are provided.…”

Section: Reviewmentioning

confidence: 99%

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

Rodriguez-Oroz

Jahanshahi

Krack

et al. 2009

The Lancet Neurology

718

464

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A dopaminergic defi ciency in patients with Parkinson's disease (PD) causes abnormalities of movement, behaviour, learning, and emotions. The main motor features (ie, tremor, rigidity, and akinesia) are associated with a defi ciency of dopamine in the posterior putamen and the motor circuit. Hypokinesia and bradykinesia might have a dual anatomo-functional basis: hypokinesia mediated by brainstem mechanisms and bradykinesia by cortical mechanisms. The classic pathophysiological model for PD (ie, hyperactivity in the globus pallidus pars interna and substantia nigra pars reticulata) does not explain rigidity and tremor, which might be caused by changes in primary motor cortex activity. Executive functions (ie, planning and problem solving) are also impaired in early PD, but are usually not clinically noticed. These impairments are associated with dopamine defi ciency in the caudate nucleus and with dysfunction of the associative and other non-motor circuits. Apathy, anxiety, and depression are the main psychiatric manifestations in untreated PD, which might be caused by ventral striatum dopaminergic defi cit and depletion of serotonin and norepinephrine. In this Review we discuss the motor, cognitive, and psychiatric manifestations associated with the dopaminergic defi ciency in the early phase of the parkinsonian state and the diff erent circuits implicated, and we propose distinct mechanisms to explain the wide clinical range of PD symptoms at the time of diagnosis.

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Akinesia in Parkinson's disease

Cited by 150 publications

References 0 publications

Primary progressive freezing gait

Primary progressive freezing gait

Motor Control Abnormalities in Parkinson's Disease

Initial clinical manifestations of Parkinson's disease: features and pathophysiological mechanisms

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