Does the Golem Feel Pain? Moral Instincts and Ethical Dilemmas Concerning Suffering and the Brain.

Pain has variously been used as a means of punishment, extracting information, or testing commitment, as a tool for education and social control, as a commodity for sacrifice, and as a draw for sport and entertainment. Attitudes concerning these uses have undergone major changes in the modern era. Normative convictions on what is right and wrong are generally attributed to religious tradition or to secular-humanist reasoning. Here, we elaborate the perspective that ethical choices concerning pain have much earlier roots that are based on instincts and brain-seated empathetic responses. They are fundamentally a function of brain circuitry shaped by processes of Darwinian evolution. Social convention and other environmental influences, with their idiosyncrasies, are a more recent, ever-changing overlay. We close with an example in which details on the neurobiology of pain processing, specifically the question of where in the brain the experience of pain is generated, affect decision making in end-of-life situations. By separating innate biological substrates from culturally imposed attitudes (memes), we may arrive at a more reasoned approach to a morality of pain prevention.

Tissue resonance analysis; a novel method for noninvasive monitoring of intracranial pressure. Technical note.

A number of noninvasive methods used to measure intracranial pressure (ICP) have been proposed in the literature. For a variety of reasons, however, none of these have displayed significant practical applicability. The authors describe their development of a new, computerized, portable device based on tissue resonance analysis (TRA) technology for the noninvasive monitoring and measurement of ICP. In response to the heart beat, the soft tissue and fluid compartments of the brain each exhibit characteristic vibration and mechanical resonant responses that radiate through the organs and tissues of the body. Patterns of vibration and mechanical resonance of various body organs and tissues are different and provide the possibility of extracting new and specific information in a noninvasive fashion. According to the TRA approach, ICP is dependent on the value of the dominant secondary (mechanical) resonance level of brain tissue. By digitally processing a reflected ultrasound signal (by using a concave ultrasonography probe with a carrier frequency of 1 MHz) from the third ventricle, the authors obtained a digital high-resolution echopulsogram, which visually is equivalent to ICP waves that are obtained invasively. The fast Fourier relationship of electrocardiogram and echopulsogram waves allowed the derivation of the secondary mechanical resonance levels. The authors developed a formula for a quantitative, noninvasive measurement of ICP, which uses information regarding multiple components of the intracranial space-both mechanical (secondary resonance) and physiological (time required for transfer of arterial blood to venous blood through brain tissue)-and the relationship between these components. A comparison of invasive and noninvasive ICP measurements was made during blinded trials in 40 patients with various diseases of the central nervous system, and ranges of ICP were measured from I to 66 mm Hg. The ICP values obtained using the two methods were highly correlated (r = 0.99), without a statistically significant difference between simultaneously obtained readings (p = 1). By using an integrative approach that reflects all components of the intracranial compartment, TRA allows for accurate noninvasive recordings of ICP. This method has significant advantages over other noninvasive technologies reported to date.

Mechanism of trigeminal neuralgia: an ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery.

OBJECT: Recent progress in the understanding of abnormal electrical behavior in injured sensory neurons motivated an examination, at the ultrastructural level, of trigeminal roots of patients with trigeminal neuralgia (TN). METHODS: In 12 patients biopsy specimens of trigeminal root were obtained during surgery for microvascular decompression. Pathological changes in tissue included axonopathy and axonal loss, demyelination, a range of less severe myelin abnormalities (dysmyelination), residual myelin debris, and the presence of excess collagen, including condensed collagen masses in two cases. Within zones of demyelination, groups of axons were often closely apposed without an intervening glial process. Pathological characteristics of nerve fibers were clearly graded with the degrees of root compression noted at operation. Pain also occurred, however, in some patients who did not appear to have a severe compressive injury. CONCLUSIONS: Findings were consistent with the ignition hypothesis of TN. This model can be used to explain the major positive and negative symptoms of TN by axonopathy-induced changes in the electrical excitability of afferent axons in the trigeminal root and of neuronal somata in the trigeminal ganglion. The key pathophysiological changes include ectopic impulse discharge, spontaneous and triggered afterdischarge, and crossexcitation among neighboring afferents.

Cranial root injury in glossopharyngeal neuralgia: electron microscopic observations. Case report.

Optical and electron microscopic examinations were made of a biopsy sample of the ninth and 10th cranial nerves obtained during posterior fossa surgery for the relief of pain in a patient suffering from glossopharyngeal neuralgia (GN). Pathological findings, which were restricted to a small fraction of fascicles in the nerves, included large patches of demyelinated axons in close membrane-to-membrane apposition to one another and zones of less severe myelin damage (dysmyelination). These observations, in the light of similar morphological changes observed in biopsy samples excised from patients with trigeminal neuralgia, and new information on the pathophysiological characteristics of injured peripheral nerve axons, can account for much of the symptomatology of GN.

Pathophysiology of trigeminal neuralgia: the ignition hypothesis.

There are no satisfactory animal models of trigeminal neuralgia, and it is difficult to obtain essential data from patients. However, trigeminal neuralgia presents with such idiosyncratic signs and symptoms, and responds to so distinctive a set of therapeutic modalities, that scientific deduction can be used to generate likely hypotheses. The ignition hypothesis of trigeminal neuralgia is based on recent advances in the understanding of abnormal electrical behavior in injured sensory neurons, and new histopathologic observations of biopsy specimens from patients with trigeminal neuralgia who are undergoing microvascular decompression surgery. According to the hypothesis, trigeminal neuralgia results from specific abnormalities of trigeminal afferent neurons in the trigeminal root or ganglion. Injury renders axons and axotomized somata hyperexcitable. The hyperexcitable afferents, in turn, give rise to pain paroxysms as a result of synchronized afterdischarge activity. The ignition hypothesis accounts for the major positive and negative signs and symptoms of trigeminal neuralgia, for its pathogenesis, and for the efficacy of treatment modalities. Proof, however, awaits the availability of key experimental data that can only be obtained from patients with trigeminal neuralgia.