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Nerve Nuclei (nerve + nucleus)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Review: Neuropathology of acute phase encephalitis lethargica: a review of cases from the epidemic period

NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2009
L. L. Anderson
Introduction: Encephalitis lethargica (EL), an epidemic disease of the early 20th century, has continued to be diagnosed sporadically since that time, including a report of 20 new cases in 2004. Many of the recent case reports state that the primary neuropathology of acute EL consists of inflammatory changes and lesions within the midbrain, basal ganglia and substantia nigra. However, the neuropathology of acute EL cases from the epidemic period was actually much more widespread. Methods: In order to characterize the neuropathology of acute phase EL, we developed a database of EL pathology based on 112 cases from the years 1915 to 1940, of which most died within 2 weeks of EL onset. Results: Our analysis revealed that cortical damage was prevalent in 75% of the 112 cases; damage to the meninges and brainstem occurred in approximately half of the cases; and the substantia nigra was damaged in only 13% of these acute cases. We also found that after 1921, damage to cranial nerve nuclei was not reported. An analysis of the neuropathology and clinical symptoms revealed little correlation. Conclusions: Based on these findings, putative modern cases of acute EL with MRI/CT indicated lesions confined solely to the midbrain, brainstem, and/or basal ganglia should not be considered, consistent with that reported during epidemic period. [source]

Phrenic paresis,a possible additional spinal cord dysfunction induced by neck manipulation in cervical spondylotic myelopathy (CSM): A report of two cases with anatomical and clinical considerations

CLINICAL ANATOMY, Issue 3 2001
Wesley W. Parke
Abstract The clinical records of two male subjects with severe cervical spondylotic myelopathy (CSM) who developed respiratory insufficiency after the cervical manipulation involved in preoperative anesthetic intubation were examined. Their cervical imaging was analyzed with respect to the known anatomic relationships of the spinal phrenic nerve nuclei to the spondylotic compressive lesions in an attempt to provide the anatomic and pathologic rationales that may explain this phrenic paresis as a possible traumatic complication of severe CSM. Perusal of extant literature revealed extensive descriptions of CSM symptoms, but none had previously reported an associated neuromuscular weakness of the diaphragm. Magnetic resonance imaging analyses indicated that the existing degree of upper cervical cord compression, when reinforced by the additional posterior and anterior pressures consequent to cervical spinal extension and flexion, could readily account for the functional impairment of phrenic nerve neuron cells and/or their efferent fibers. Thus, the anatomic relations of the phrenic nerve nuclear columns and their efferent tracts predispose them to interference by compressive lesions found in CSM, and undue manipulation of the cervical spine when advanced stenosis is known to be present should be recognized as a possible cause of cervical spondylotic myelopathic,phrenic paresis. Clin. Anat. 1:173,178, 2001. © 2001 Wiley-Liss, Inc. [source]

A neuro-Behcet's lesion in oculomotor nerve nucleus

ACTA NEUROLOGICA SCANDINAVICA, Issue 2 2003
M. D. Aydin
Objective , Fascicular oculomotor nerve involvement is occasionally seen in Behcet's disease, but nuclear involvement is very rare. Case presentation , A 25-year-old woman presented with the Behcet's symptoms and the left eye problems. Physical examination revealed muco-cutaneous lesions, eyelid ptosis, mydriasis, upward and medial gaze palsy and lateral deviation on the left eye. Serologic tests were positive. An inflammatory lesion was detected in the left oculomotor nerve nucleus on magnetic resonance imaging. Neuro-Behcet's disease was considered the most likely diagnosis. Result , Dexamethasone treatment was ordered. Muco-cutaneal lesions, laboratory abnormalities were normalized after 1 year; but oculomotor nerve palsy persisted in spite of improvement in radiological findings. Conclusion , Clinical signs of oculomotor nerve palsy may persist despite the radiological improvement. [source]