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[Dysphagia] Lateral Medullary Syndrome - Wallenberg Syndrome


  • Subject: [Dysphagia] Lateral Medullary Syndrome - Wallenberg Syndrome
  • From: Drirenect at aol.com (Drirenect@aol.com)
  • Date: Fri May 12 06:15:57 2006

Prognosis depends on the exact site of lesion as well as extent - and the  
usual - age, gender, medications, comorbidities and so on:
 
Dysphagia in Lateral  Medullary Infarction 
(Wallenberg?s  Syndrome) 
An Acute Disconnection  Syndrome in Premotor Neurons 
Related to Swallowing  Activity?  Stroke.  2001;32:2081-2087.) 
Ibrahim Aydogdu, MD;  Cumhur Ertekin, MD; Sultan Tarlaci, MD; Bulent Turman, 
MD,  PhD; 
Nefati Kiylioglu, MD;  Yaprak Secil, MD 
Although in WS the lesion  due to LMI is unilateral, its effect on 
oropharyngeal swallowing is bilateral.  In 
LMI, primarily the premotor  neurons in the nucleus ambiguus and their 
connections seem to be affected.  Consequently, 
a disruption and/or  disconnection of their linkage to swallowing-related 
cranial motor neuron pools  bilaterally and to the 
contralateral nucleus  ambiguus could produce the swallowing disorders in WS. 
However, the remaining  intact ipsilateral 
premotor neurons and the  contralateral center in the medulla oblongata may 
eventually begin to operate  and overcome 
the severity and long-term  persistence of dysphagia.  
Dysphagia in unilateral medullary infarction 
NEUROLOGY  2005;65:714-718 
Lateral vs medial lesions  
Miseon Kwon,  PhD, Jae H. Lee, MD and Jong S. Kim, MD  
Objective: To study dysphagia in pure, unilateral  medullary infarction using 
video fluoroscopic swallowing (VFS) tests  and to compare the results between 
lateral medullary infarction (LMI) and medial medullary infarction (MMI).  
Methods: We studied 46 patients with medullary infarction  (37 LMI, 9 MMI). 
Based on the MRI findings, each LMI was  classified rostrocaudally as either a 
rostral or caudal lesion, and  horizontally as either a superficial (lateral + 
dorsal) or  nonsuperficial lesion. Each MMI was assigned to either a deep 
(lesion  extending to the dorsal surface) or superficial lesion group. VFS  
examination was conducted and an 8-point scale was used for assessing  the severity 
of dysphagia. Based on these results, dysphagia was classified as: 1) 
problems on timing of hyolaryngeal excursion (PT), and 2) problems on range of 
hyolaryngeal excursion (PR).  
Results: Dysphagia was more frequent (p < 0.05)  in MMI patients (78%) than 
in LMI patients (35%). Among the LMI  patients, dysphagia was more frequent (p 
< 0.01) and severe  (p < 0.01) in the rostral than in the cadual group and in  
the nonsuperficial than in the superficial group. In the MMI group,  there 
was no difference in the frequency of dysphagia between the  deep and 
superficial groups. Regarding the characteristics of  dysphagia, seven (54%) of the LMI 
patients had PR, five (38%) had PT,  and one (8%) had both. For the MMI 
patients, PT was frequent  (86%) but PR was present in only one patient (14%). Five 
MMI  patients (71%) showed no responses to penetration or aspiration,  and 
silent dysphagia was observed in only four LMI patients  (31%).  
Conclusions: Dysphagia is as frequent and severe in  medial medullary 
infarction (MMI) as in lateral medullary  infarction (LMI) patients. The types and 
characteristics of dysphagia  are different between the LMI and MMI patients, 
implicating the rationale for a different treatment strategy.  
  
____________________________________

Pure lateral medullary infarction: clinical?radiological  correlation of 130 
acute, consecutive patients Brain, Vol. 126, No. 8, 1864-1872, August  2003 
Jong S. Kim  
Although there have been attempts to make  clinical?MRI correlation in 
patients with lateral medullary  infarction (LMI), studies with a large number of 
patients are  unavailable. In this study, clinical features, MRI findings and  
angiogram results of 130 acute, consecutive patients with pure LMI  were 
studied and correlated. MRI-identified lesions were classified  rostro-caudally as 
rostral, middle and caudal, and horizontally as  typical, ventral, large, 
lateral and dorsal. The distribution of  horizontal subtypes was significantly 
different  (P <0.001) among three rostro-caudal lesions in that  rostral lesions 
tend to be ventral types and caudal lesions are  lateral types. Patients with 
rostrally located lesions had dysphagia,  facial paresis (P < 0.01, each) and 
dysarthria  (P < 0.05) significantly more often, and severe  gait ataxia and 
headache (P < 0.05, each) less  often than those with caudal lesions. The 
frequencies of dysphagia  (P < 0.01), dysarthria  (P < 0.01) and bilateral 
trigeminal sensory  pattern (P < 0.05) were significantly different among horizontal 
subtypes in that these symptoms were frequent in patients with ?large type? as 
compared with those with  lateral type lesions. Angiograms performed in 123 
patients showed  vertebral artery (VA) disease in 67% and posterior inferior 
cerebellar artery (PICA) disease in 10%. The presumed pathogenetic mechanisms 
included large vessel infarction in 50%, arterial dissection in 15%, small vessel 
infarction in 13% and cardiac embolism in 5%. Dissection occurred more often 
in patients with caudal (versus rostral) lesions (P < 0.01),  whereas dorsal 
type infarcts (versus other types) were related  more often to cardiogenic 
embolism and normal angiogram findings (P < 0.05, each). Patients with isolated 
PICA  disease (versus those with VA disease) more often had cardiogenic  
embolism (P < 0.05) and less often had dissection  (P < 0.01). It is concluded that 
rostro-caudal  and horizontal classification of MRI helps us to understand the  
clinical and, partly, the aetiopathogenetic aspect of the  heterogeneous LMI 
syndrome.  





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