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BRIEF COMMUNICATIONS: S. W. Seo, J. H. Heo, K. Y. Lee, W. C. Shin, D. I. Chang, S. M. Kim, and K. Heo Localization of Claude’s syndrome Neurology 2001; 57: 2304-2307 [Abstract] [Full text] [PDF]

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Reply to Dr. Coppola's letter to the Editor

Ji Hoe Heo   (1 March 2002)

Localization of Claude’s syndrome

Robert J Coppola   (1 March 2002)

Reply to Dr. Coppola's letter to the Editor 1 March 2002
Ji Hoe Heo yonsei University College of Medicine Seoul Korea Send Correspondence to journal: Re: Reply to Dr. Coppola's letter to the Editor jhheo{at}yumc.yonsei.ac.kr Ji Hoe Heo	We appreciate Dr. Coppola’s comments. Our findings clearly showed that lesions of the superior cerebellar peduncle just below and medial to the red nucleus is responsible for Claude’s syndrome. [1] To our best knowledge, no cases with isolated lesions confined to the red nucleus have been reported to present as Claude’s syndrome. In the case described by the author, lesions were not confined to the red nucleus or midbrain but were extended to the subthalamic nucleus, and the inferior thalamus. [2] Cerebellar ataxia can occur by lesions of the dentatothalamic fibers at any level from the midbrain to the thalamus. In the midbrain at the red nucleus level, a lesion may produce both ataxia and oculomotor nerve palsy. However the lesion should be large enough to damage both oculomotor nerve fascicles and dentatothalamic fibers that run outside the red nucleus. [3] We agree that imaging studies may not be the ultimate determinant in correlating the site of pathology with clinical syndromes. However, pathological examinations are impractical in most patients with clinical syndromes of mild neurologic deficits such as Claude’s syndrome. In addition, pathologic examinations of the lesion may not be performed at the same time as a patient was demonstrating clinical features. In the author’s case, for example, clinical features of Claude’s syndrome were correlated with pathological findings obtained two years later. [2] It is uncertain whether the patient still had typical clinical features of the syndrome at the time of pathologic examinations. Dynamic biochemical, functional, and morphological changes occur in ischemic tissues during the acute stage of cerebral infarctions, which are the most common cause of Claude’s syndrome. Timely examined imaging studies while a patient is demonstrating typical clinical features of Claude’s syndrome may provide real-time morphological reflections on the functional deficits. Current MRI technologies are good enough to delineate the brainstem structures. The red nucleus and its relation to infarctions were nicely shown in our paper. [1] Regarding the issue of heparin used in our patients, no studies are available to conclude the efficacy or safety of heparinization in patients with small cerebral infarctions. [4] However, intravenous t-PA, which may carry higher risk of hemorrhages than heparin, has been reported to be safe and effective in lacunar infarctions. In our institute, intravenous heparin has long been safely used in selected patients with atherothrombotic and lacunar infarctions as well as in those with cardioembolic infarctions under the strict titration of doses. References: 1. Seo SW, Heo JH, Lee KY, Shin WC, Chang DI, Kim SM, Heo K. Localization of Claude’s syndrome. Neurology 2001;57:2304-2307. 2. Coppola RJ, Freedman H. Bilateral Claude syndrome: clinical and neuropathological study. Buckeye Osteopathic Physician 1991;60(8):4-6. 3. Haines DE. Neuroanatomy: An Atlas of Structures, Sections, and Systems, 4th ed. Baltimore-Munich: Urban & Schwarzenberg, 1995. 4. Fischer CM. A Career in cerebrovascular disease: a personal account. Stroke 2001;32:2719-2724.
Localization of Claude’s syndrome 1 March 2002
Robert J Coppola Florida Neurovascular Institute Tampa FL Send Correspondence to journal: Re: Localization of Claude’s syndrome rjcoppola1{at}aol.com Robert J Coppola	Seo et al. revisit Claude’s syndrome, reviewing a small number of reported cases and adding six cases of their own. [1] A recurring theme is the notion that the red nucleus is not a major site of neuropathology in the genesis of this relatively rare brainstem syndrome. This is based predominantly on MRI imaging of their six cases and inclusion of eight previously reported cases. I refer the authors and readers to our case study of a patient presenting with bilateral Claude’s syndrome. [2] This patient presented with acute complete bilateral third nerve palsies, bilateral cerebellar ataxia, and absence of pyramidal tract signs. Computed tomography scanning was the chief diagnostic tool at the time this stroke occurred and demonstrated a hypodense midline lesion in the midbrain. On pathological examination multiple coronal sections showed infarctions in the midline, involving the inferior thalamus and also the area of the subthalamic nucleus. The lesion, confirmed by microscopic examination, extended directly into the midbrain and involved the midportion of the raphe and extended into the red nucleus area on both sides. Our study thus does not support the minimization of the red nucleus as an important site of pathology in this syndrome. Additionally, of the eight cases not excluded from their article review of eighteen, two pathologically examined cases (it is unclear to me if these are the only direct tissue studies, but such seems implied) also showed red nucleus involvement. As a neurologist whose practice predates the advent of routine MRI imaging I wish to state the obvious. The ultimate determination in correlating sites of pathology with clinical syndromes must be based on tissue examination and not solely on black and white two-dimensional images. Additionally, neurotherapeutic intervention must first involve rational, justified, and, above all, safe means. Without a stated cardiac rationale I question the initial use of IV heparin in five of the six patients. References: 1. Seo SW, Heo JH, Lee KY, Shin WC, Chang DI, Kim SM, Heo K.Localization of Claude’s syndrome. Neurology 2001 ; 57: 2304-2307. 2. Coppola RJ, Freedman H. Bilateral Claude syndrome: clinical and neuropathological study. Buckeye Osteopathic Physician 1991; 60 (8): 4-6.