Evoked potentials in clinical medicine , Evoked potentials in clinical medicine , کتابخانه مرکزی دانشگاه علوم پزشکی ایران

Evoked Potentials in Clinical Medicine

The practice and theoretical basis of pain measurement is reviewed and critically examined in the areas of animal research, human subjects laboratory investigation and clinical study. The advantages and limitations of both physiological and behavioral methods are discussed in each area, and subjective report procedures are evaluated in human laboratory and clinical areas. The need for procedures that bridge these areas is emphasized and specific issues are identified. Progress in the technology of pain measurement over recent decades is reviewed and directions for future work are suggested.

Pain measurement: an overview

Evoked potentials in clinical medicine (second of two parts).

There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. Other causes of trigeminal neuralgia in which demyelination is involved or implicated include multiple sclerosis and, probably, compressive space-occupying masses in the posterior fossa. Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. Similar foci of nerve root demyelination and juxtaposition of axons have been demonstrated in multiple sclerosis patients with trigeminal neuralgia. Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation. Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. The role of remyelination in initial symptomatic recovery after decompression is unclear. However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. In addition to causing symptomatic relief, vascular decompression leads to rapid recovery of nerve conduction across the indented root, a phenomenon that, we suggest, is likely to reflect the reversal of compression-induced conduction block in larger myelinated fibres outside the region of demyelination. Trigeminal neuralgia can occur in association with a range of other syndromes involving vascular compression and hyperactivity of cranial nerves. Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.

/pdf/trigeminal-neuralgia-pathology-and-pathogenesis-46wd3umhrm.pdf

Trigeminal neuralgia: pathology and pathogenesis.

As we age, our arteries elongate and our brains "sag." As a consequence of these processes, redundant arterial loops and bridging or intrinsic hindbrain veins may cause cross-compression of cranial nerve root entry zones in the cerebellopontine angle. This pulsatile compression can be seen to produce hyperactive dysfunction of the cranial nerve. Symptoms of trigeminal or glossopharyngeal neuralgia (somatic sensory), hemifacial spasm (somatic motor), tinnitus and vertigo (special sensory) and some cases of "essential" hypertension are caused by these vessels compressing cranial nerves V, IX--X, VII, VIII, and left X and medulla oblongata. Using microsurgical techniques, the symptoms may be relieved by vascular decompression, findings and results in 695 paients are briefly reviewed and correlated. A chronic primate model of "essential" hypertension is briefly described.

Neurovascular compression in cranial nerve and systemic disease.

Intracranially recorded responses from the human auditory nerve: New insights into the origin of brain stem evoked potentials (BSEPs)

Trigeminal evoked potentials in humans

Effects of compression and ischemia on spinal cord evoked potentials

• The mechanism by which glycerol abolishes the pain of tic douloureux with minimal trigeminal deafferentation remains unknown. To study the action of glycerol, ten cats underwent unilateral retrogasserian injection of anhydrous glycerol. The contralateral (control) side was injected with saline. Glycerol injection increased the average latencies and reduced the average amplitudes of trigeminal brain-stem evoked potentials. Histopathologic examination disclosed focal demyelination, axonal swelling, endoneurial fibrosis, and neuronal loss. Evoked potentials were severely altered or abolished in cats with axonal damage in the maxillary portion of the postganglionic nerve. Glycerol injection into the trigeminal nerve damages axons and myelin sheaths. We believe that relief of tic douloureux after glycerol injection most likely results from further destruction of the abnormally myelinated fibers implicated in the etiology of trigeminal neuralgia.

Experimental Trigeminal Glycerol Injection: Electrophysiologic and Morphologic Effects

Clinical and experimental brain retraction pressure monitoring.

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