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Letters |
University Laboratory of Physiology
Oxford University
Oxford,
England
It was with great interest that we studied the case reports in the article titled "Midbrain Ataxia: An Introduction to the Mesencephalic Locomotor Region and the Pedunculopontine Nucleus" [1] that appeared in the March 2005 issue of the AJR. The authors state that the lesions are located in the pedunculopontine nucleus (PPN), and they draw neurologic conclusions from this. However, the lesions illustrated appear to be in the midbrain well above and medial to the PPN; hence, the conclusions are misleading. The lesions appear to involve the periaqueductal gray area and possibly the posterior hypothalamus. Thus, the ataxia they describe could be more rationally ascribed to sensory deficits.
The discussion is fairly misguided as a result and might lead others to misdiagnose the cause of midbrain ataxias.
References
Geffen School of Medicine
University of California Los Angeles
Medical Center
Los Angeles, CA 90095
West Los Angeles Veterans Affairs
Medical Center Los Angeles, CA
90073
We read with interest the letter of Drs. Aziz et al., and we thank them for their input.
Our article [1], in order of importance, sought to make the following points. First, although ataxia is usually associated with the cerebellum, we wished to review a less familiar but important cause—lesions of the dorsal midbrain tegmentum—and to stress that the dorsal midbrain should be a focus area in patients presenting with gait ataxia, especially when accompanied by third-nerve deficits or vertical gaze palsy. We acknowledge that this association has been previously described in the neurology literature under other names such as "Claude's syndrome" and "Nothnagel's syndrome" [2], but this association is now largely ignored or forgotten.
Second, we suggest that since these descriptions were first published in the literature, neuroanatomists have discovered and described a region of the dorsal midbrain known as the mesencephalic locomotor region. This discovery makes the original descriptions from the turn of the last century more relevant because it gives them an anatomic underpinning. To date, there is no clear definition of the boundary of the mesencephalic locomotor region and which cell groups should be included in the mesencephalic locomotor region. On the basis of previous physiologic studies, we propose that components of the mesencephalic locomotor region should include several cell groups that appear to be essential for locomotion, produced under several different behavioral circumstances, including at least the periaqueductal gray matter, cuneiform nucleus, pedunculopontine nucleus (PPN), and locus ceruleus. The patients presented in our article have lesions that involve the putative area of the mesencephalic locomotor region.
Finally, and of least priority because it cannot be specifically visualized with MRI, we hypothesize that the lesions also involve the PPN, a major component of the mesencephalic locomotor region. Our hypothesis is based on lesion location and clinical correlation with the functions of the PPN. However, the issue of the location of the PPN is important for the sake of accuracy. The PPN is a heterogeneous population of neurons lying in the dorsal midbrain as part of the mesencephalic reticular formation. Definition of the PPN area is based on induction of locomotor activity by either electrical or chemical stimulation of the tegmental area. Therefore, it will be difficult to argue precisely exactly which lesions involve the PPN on the basis of MRI findings.
In the human brain, the PPN is bordered medially by fibers of the superior cerebellar peduncle and peduncular decussation and is bordered laterally by the medial lemniscus. Rostrally, the anterior portion of the PPN contacts the substantia nigra and is adjacent to the retrorubral field, whereas the most caudal pole is adjacent to the locus ceruleus [3]. Thus, to locate this nucleus, which has a significant rostrocaudal extent in the midbrain, it is most accurate to rely on these landmarks rather than on schematics from neuroanatomy drawings, which may be imprecise. We do not claim that the lesions shown are at the epicenter of the PPN, and we agree with Aziz et al. that the epicenter of the lesions in our cases is slightly superior and medial to the location of the PPN shown in some neuroanatomic diagrams. However, given the anatomic landmarks of the PPN described and the extent of our lesions, we believe that the lesions shown do extend to involve the PPN. The interested reader may refer to labeled brain sections and the previously mentioned landmarks [4].
Finally, regarding the statement by Aziz et al. that the lesions shown may be located in the posterior hypothalamus, we believe that the images clearly show them in the dorsal midbrain tegmentum, and we point out that animal experiments suggest that it is the lateral (and not dorsal) hypothalamus that is thought to be involved in locomotion [5].
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