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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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