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• Is freezing in Parkinson's disease a visual-motor hyperfunction?
  Dorothy Cowie
  Published on: 30 November 2010

• Published on: 30 November 2010

  Is freezing in Parkinson's disease a visual-motor hyperfunction?

  • Dorothy Cowie
  • Other Contributors:
    • Brian L Day

  Dear Editor,

  The article 'Disorders of Visual Perception' (ffytche, Blom & Catani, JNNP 2010;81:1280-1287) presents an interesting new classification of disorders of visual perception. It describes a wide range of disorders whose sources are cortical or subcortical rather than due to diseases of the eye. Each is classified as a disorder of one brain region (topological disorders) or of connectivity between re...

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  Dear Editor,

  The article 'Disorders of Visual Perception' (ffytche, Blom & Catani, JNNP 2010;81:1280-1287) presents an interesting new classification of disorders of visual perception. It describes a wide range of disorders whose sources are cortical or subcortical rather than due to diseases of the eye. Each is classified as a disorder of one brain region (topological disorders) or of connectivity between regions (hodological disorders); and as reflecting a decrease (hypofunction) or increase (hyperfunction) in function. The disorders are also divided by different types of visual function, such as disorders of visual memory or visual attention. One of few 'empty cells' in the framework is an example of a visual motor, topological hyperfunction. On the basis of work from our laboratory and others, we would like to argue that a good example for this cell is over- reactions to visual information for locomotion in Parkinson's disease (PD).

  This topic came to our attention through the phenomenon of 'freezing' in PD. A freeze occurs when a patient is unable to walk despite wanting to do so: subjectively, the patient feels as if he is 'glued to the floor'. Freezing has long been associated with unusual responses to visual stimuli. In paradoxical kinesia, a freeze is unblocked, or short strides lengthened, by vision of transverse lines on the floor (Azulay et al, 1999). Patients who freeze ('freezers') show large responses to visual optic flow information in a balance task (Bronstein et al, 1990). We have recently shown that these patients also slow down dramatically when passing through doorways (Cowie et al, 2010). Whereas healthy controls slowed to a degree inversely proportional to door width (allowing accurate passage), freezers did so to a dramatic extent. Each visually specified change in door width elicited a larger drop in velocity for PD freezers than for healthy controls. The patients had no difficulties in explicitly judging the width of door, and the extent of slowing was not predicted by simpler motor abilities such as turning. Rather, the result indicates that responses to action-relevant visual information about door width were exaggerated in this group. This theory resolves the apparent paradox that visual information can help or hinder walking depending on the circumstance. Current evidence suggests that these effects are specific to freezers, since other patients with PD are not susceptible to such effects (Almeida & Lebold, 2010).

  From these results showing over-responses to visual information, we can argue that our visual motor disorder is one of hyperfunction. What of its neural basis? Visual control of action activates a network of brain areas including the dorsal stream, premotor cortices and cerebellum. However, a SPECT study (Hanakawa et al, 1999) suggests that one specific area is involved in hypersensitive locomotor responses to visual information. In this study freezers and non-freezers walked on a treadmill with lines painted parallel or transverse to the direction of walking. As expected, the PD group had exaggerated responses to transverse lines, a form of 'paradoxical kinesia'. When comparing the brain response to transverse and parallel lines, only the right lateral premotor cortex (PMC) was more active in PD patients than in controls. Thus this area seems to be the focus of the over-reaction to action-relevant visual information in walking in PD freezers. Within ffytche et al's framework we would therefore classify over-reactions to visual information for locomotion in Parkinson's disease (PD) as a topological disorder of hyperfunction, specifically of the lateral premotor cortex.

  Of course this classification is subject to the same limitations that the authors acknowledge in their article. Though the behaviour we measure is a 'hyperfunction', it coexists with other disease symptoms which are certainly 'deficits' in ffytche et al's terms. The primary disturbance in PD is the dopaminergic deficit in the striatum. Though there is little literature on the subject, a possibility is that over-reactions to visual information (and indeed freezing of gait) in PD are a direct result of this deficit. This would mean PMC hyperfunction is a downstream result of a basal ganglia deficit. Clearly, this makes the classification scheme more ambiguous than it first appears. Furthermore, though Hanakawa et al's study shows one clear focus of overactivation, this may result from damage to networks of areas including connections between the PMC and its sensory input areas or motor output areas.

  Nevertheless, a clear strength of ffytche et al's framework is that novel disorders can be brought within its structure. This allows consideration of the novel disorder within a broader context at the same time as fleshing out the model. We argue that visual control of locomotion in Parkinson's disease (PD) can be considered this way, and look forward to further discussions surrounding the framework and its contents.

  Yours sincerely

  Dr Dorothy Cowie, Goldsmiths, University of London

  Prof Brian L Day, UCL Institute of Neurology

  References

  Azulay, J., Mesure, S., Amblard, B., Blin, O., Sangla, I.,& Pouget, J. (1999). Visual control of locomotion in Parkinson's disease. Brain, 122, 111-20.

  Bronstein, A. M., Hood, J. D., Gresty, M. A., & Panagi, C. (1990). Visual control of balance in cerebellar and Parkinsonian syndromes. Brain, 113, 767-79.

  Cowie D, Limousin P, Peters A, & Day BL. (2010). Insights into the neural control of locomotion from walking through doorways in Parkinson's disease. Neuropsychologia, 48, 2750-57.

  Almeida QJ, & Lebold CA. (2010). Freezing of gait in Parkinson's disease: a perceptual cause for a motor impairment? J Neurol Neurosurg Psychiatry, 81, 513-18.

  Hanakawa T, Fukuyama H, Katsumi Y, Honda M, & Shibasaki H. (1999). Enhanced lateral premotor activity during paradoxical gait in Parkinson's Disease. Ann Neurol, 45, 329-36.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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