Dear Editor,

I recently read the article by Satoh and colleagues (1) with great interest and have the following question and comments for authors. Their right handed violinist patient became unable to coordinate the movements of bowing and fingering hands as a result of a callosal infarct affecting the entire anterior aspect of the callosum per MRI. From what appears in the figure, as published, the splenium per se seems intact. This, however, is a mute point in view of forthcoming observations.

Now, the question: Since the directionality of sensory callosal traffic in a right hander is from the minor (right) to the major (left) hemisphere (2), it is hard to understand the sensory defects detected on the right side of the body as depicted in section "examination of callosal functions." This may have been a typographical or clerical error and if so it would be important to correct it for readers (or explain it).

Second, the authors statement, “left fingers require finer movements than the right, as they press the violin strings,” displays unfamiliarity with playing a string instrument and overlooks the critical role of the right hand in allowing production of sounds by the fingering hand (i.e. violin playing requires very fine tuning of movements by the bowing hand); since movements of bowing hand must precede those the fingering (by an interhemispheric transfer time, (IHTT)) to allow vibration of the strings if sounds are be made by fingering the strings. This has been documented in the past (2, 3).

According to the one-way callosal traffic circuitry underpinning the lateralities of motor and sensory control (2, 4, 5), their patient’s “left hemianopia for musical symbols,” displayed in tachistoscopic examinations, was in fact due to patient’s difficulty in moving his eyes to the left in the time allowed, as documented in patients with callosotomy (6, Fig. 7) rather than to a role by the splenium of the corpus callosum in vision (4, 6).

References

1. Satoh M, Furukawa, Takeda K, Kuzuhara S.
Left hemianopia of musical symbols caused by callosal infarction.
J Neurol Neurosurg Psychiatry 2006; 77: 705-706.

2. Derakhshan I.
Crossed-uncrossed difference (CUD) in a new light: anatomy of the negative CUD in Poffenberger's paradigm.
Acta Neurol Scand. 2006; 113:203-208.

3. Baader AP, Kazennikov O, Wiesendanger M.
Coordination of bowing and fingering in violin playing.
Brain Res Cogn Brain Res. 2005; 23:436- 443.

4. Derakhshan I.
Nature's shell game revealed: evidence for non- Newtonian laterality of macular vision (Ocular integration in the human visual cortex.
Can J Ophthalmol. 2007; 42:485-486.

5. Derakhshan I.
How do the eyes move together? New understandings help explain eye deviations in patients with stroke.
CMAJ. 2005; 172:171- 173.

6. Holtzman JD.
Interactions between cortical and subcortical visual areas: evidence from human commissurotomy patients.
Vision Res. 1984; 24:801-813.

Dear Editor,

In their recent paper, Best and colleagues (1) provided evidence to support an emerging hypothesis about how interactions between neurotologic and psychiatric factors may determine the clinical course of chronic dizziness. Investigators since the 1980s have presumed a direct correlation between type and severity of vestibular dysfunction and psychiatric morbidity, which has not been demonstrated with any consistency. In contrast, retrospective (2) and prospective (3) data suggest that psychiatric risk factors and pre - existing psychiatric illnesses are important determinants of outcome in patients who develop chronic dizziness. This newer construct suggests that inherent psychological vulnerabilities, particularly to anxiety, may be just as important as type and severity of neurotologic illness in determining long-term morbidity.

Best and colleagues are quite right to conclude that isolated, non-specific findings on peripheral vestibular function tests have been overemphasized, both clinically and in research studies. These test results appear to have little significance in the absence of supporting clinical history or examination findings. Integrative tests such as the sensory organization test (SOT) may reveal more about normal and dysfunctional balance strategies used by patients with persistent dizziness, though the contributions of neurotologic and psychiatric factors to SOT performance are still being investigated.

Several aspects of this paper require clarification. It is not clear how patients were assigned to the anxiety, depression, and somatization (A,D,S) groups. Did subjects in these groups have no evidence whatsoever of neurotologic illness or no evidence of active vestibular dysfunction? This is an important distinction because neurotologic events may trigger de novo psychiatric disorders or exacerbate pre-existing psychiatric illnesses even if patients fully compensate for past vestibular deficits (2,3). Therefore, it is not clear if subjects in the A,D,S groups had primary psychiatric causes of dizziness, secondary psychiatric disorders, or exacerbations of pre-existing psychiatric conditions that persisted after full recovery from previous neurotologic illnesses.

The authors measured psychiatric symptoms during different states of the various neurotologic illnesses. Patients underwent psychosomatic examinations during the acute phase of vestibular neuronitis compared to neurotologically quiescent periods of Meniérè’s disease and vestibular migraine. Patients with histories suggesting BPPV were excluded if their Dix- Hallpike tests were negative, potentially eliminating individuals with psychiatric sequelae from recent or intermittent bouts of BPPV. Therefore, accurate interpretations of differences in psychiatric morbidity across neurotologic conditions cannot be made from these cross-sectional measurements. In addition, the paper reports data on psychiatric symptoms, not psychiatric disorders; therefore, statements about the lack of a relationship between vestibular findings and specific anxiety disorders (e.g., agoraphobia) are not supported by the results contained in the manuscript.

Notwithstanding these questions and comments, Best and colleagues deserve commendation for their final conclusion that the evaluation of patients with chronic dizziness must advance beyond hierarchical, dichotomous thinking in which physicians pursue extensive neurotologic evaluations first, consider psychiatric conditions only after time-consuming neurotologic interventions have failed, and miss the medical-psychiatric comorbidity that exists across a wide spectrum of neurotologic illnesses.

References

1. Best C, Eckhardt-Henn A, Diener G, Bense S, Breuer P, Dieterich M. Interaction of somatoform and vestibular disorders J. Neurol. Neurosurg. Psychiatry 2006;77;658-664.

2. Staab JP, Ruckenstein MJ. Which comes first? Psychogenic dizziness versus otogenic anxiety. Laryngoscope 2003;113:1714–18.

3. Godemann F, Schabowska A, Naetebusch B, Heinz A, Strohle A. The impact of cognitions on the development of panic and somatoform disorders: a prospective study in patients with vestibular neuritis. Psychol Med. 2006; 36:99–108.

Competing interests: None.

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

Dear Editor,

I am looking for others with stroke ataxia - this movement disorder has been with me since I had an aneurysm burst in my cerebellum 14 years ago. Although I have found ways of compensating for the deficits I feel there must be research information available which I hope to find.

Please contact me if your ataxia is not of genetic origin.

I belong to Internaf, where the medical information is excellent - but the primary focus is the genetic ataxias.

My email address is: jkp26@cox.net.

Jillian