wallerian degeneration/hypoxia

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Rapid loss of motor nerve terminals following hypoxia-reperfusion injury occurs via mechanisms distinct from classic Wallerian degeneration.

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Motor nerve terminals are known to be vulnerable to a wide range of pathological stimuli. To further characterize this vulnerability, we have developed a novel model system to examine the response of mouse motor nerve terminals in ex vivo nerve/muscle preparations to 2 h hypoxia followed by 2 h

Spatiotemporal distribution of spectrin breakdown products induced by anoxia in adult rat optic nerve in vitro.

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Hypoxic/ischemic and traumatic injury to central nervous system myelinated axons is heavily dependent on accumulation of Ca ions in the axoplasm, itself promoted by Na influx from the extracellular space. Given the high density of nodal Na channels, we hypothesized that nodes of Ranvier might be

Experimental carbon monoxide leucoencephalopathy in the cat.

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After left common carotid artery ligation, cats were exposed to different CO gas concentrations for different periods, and the cerebral lesions were examined by light and electron microscopy at different intervals after exposure. Exposure to the higher concentration produced severe cardiopulmonary

Neurogenic bladder due to hypoxic-ischemic demyelination.

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OBJECTIVE Hypoxia is commonly known to target neuronal cell bodies. Although myelin is a non-infrequent target, posthypoxic demyelination is a rarely described entity. We describe the case of a man who developed neurogenic bladder following a motor vehicle accident. METHODS Following a severe

[Treatment of peripheral facial paralysis with ultrasound].

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In a survey on the onset of peripheral facial paralysis, the roll of hypertension in the stylomastoid canal compressing the facial nerve is underlined. Intracanalicular hypertension is due to edema resulting from capillary vasodilatation, secondary to anoxia due to a regional vasospasm. When return

[Electrophysiological study on pathophysiology of Bell's palsy--distribution of nerve conduction velocities (DNCV) in facial nerve with collision method].

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The etiology of Bell's palsy is still obscure, but the hypothesis that hypoxia and compression of the nerve induced by edema in the Fallopian canal are the main causes of Bell's palsy is widely accepted. Tojima (1988) reported that the motor nerve conduction velocity (MCV) gradually decreased as

Imaging corticospinal degeneration in neonatal rats with unilateral cerebral infarction.

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Recent human studies indicate that magnetic resonance (MR) imaging, particularly diffusion weighted imaging, detects abnormalities within the descending cortico-spinal tract following stroke. Whether these changes are directly related to processes of axonal degeneration and how MR changes (e.g.

Diagnosis, physiology, pathology and rehabilitation of traumatic brain injuries.

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Accumulating clinical and experimental studies continue to elucidate and further define the significance of intra- and extra-cranial factors which determine outcome of traumatic brain injury. These factors include severity of injury, age of the patient, presence or absence of premorbid brain

Complications: neuropathy, pathogenetic considerations.

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The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy, often accompanied by autonomic neuropathy. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration,

Cellular correlates of longitudinal diffusion tensor imaging of axonal degeneration following hypoxic-ischemic cerebral infarction in neonatal rats.

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Ischemically damaged brain can be accompanied by secondary degeneration of associated axonal connections e.g. Wallerian degeneration. Diffusion tensor imaging (DTI) is widely used to investigate axonal injury but the cellular correlates of many of the degenerative changes remain speculative. We

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