Spinal Cord Injury, Softcover reprint of the original 1st ed. 1982

We shall not, and those who come after us must not, accept the goals that were not reached yesterday as unsurmountable today or tomorrow. We will strive to render the world of the paralyzed-on-wheels but a transitory stop, and settle for nothing short of optimal recovery. N. Eric Naftchi In man, the process of "encephalization" culminates in almost complete control of the brain over the lower centers. Transection of the spinal cord severs the extensions of its nerve fiber tracts running to and from various brain centers. Although there is some confusion on the meaning of spinal shock, it is supposed to last from two to three weeks or longer in man, compared with less than a few minutes in the frog. This is a testimony to the complexity of the suprasegmental control in higher animals. Since the brain exerts its control over the internal environment through several monoamine, amino acids, and peptide neurotransmitters, it should not be surprising if the metabolism of these transmitters is found to be drastically altered along with other physical and metabolic dysfunctions which ensue following the spinal cord section. In spite of the major strides in rehabilitation of traumatic spinal cord injury, our knowledge of the etiology underlying the diverse neurophysiologic derangements remains limited. For instance, we are just becoming aware of some of the changes in the "milieu interieur.

Section One: Molecular Mechanisms of Acute Traumatic Spinal Cord Injury.- 1. Glial Fibrillary Acidic Protein (GFA) and Neuroglial Scarring, A Review.- 2. Positive and Negative Contrast Myelograph in Spinal Trauma.- 3. Effect of Pharmacological Agents on Normalization of Molecular and Histologic Dysfunction Following Traumatic Injury to the Spinal Cord.- 4. Molecular Pathogenesis of Spinal Cord Degeneration after Traumatic Injury.- Section Two: Sequelae of Spinal Cord Injury: Possible Mechanisms of Spasticity and Pain Perception.- 5. Changes in the CNS Biogenic Amines and Tyrosine Hydroxylase Activity after Spinal Cord Transection in the Rat.- 6. Brain Catecholamines, Serotonin, and Gamma-Aminobutyric Acid and Adrenal Catecholamines after High Spinal Cord Transection in the Rat.- 7. Substance P and Leucine-Enkephalin Changes in Spinal Cord of Paraplegic Rats and Cats.- 8. Quarternary and Monoamine Imbalance after Spinal Transection (A Possible Mechanism of Spasticity).- 9. Alterations of Various Physiological and Biochemical Parameters during the Development of Spasticity in the Chronic Spinal Cat.- 10. Clinical Trial of an Alpha Adrenergic Receptor Stimulating Drug (Clonidine) For Treatment of Spasticity in Spinal Cord Injured Patients.- Section Three: Hemodynamic Changes During Autonomic Dysreflexia.- 11. Relationship Between Serum Dopamine-?-Hydroxylase Activity, Catecholamine Metabolism, and Hemodynamic Changes during Paroxysmal Hypertension in Quadriplegia.- 12. Autonomic Hyperreflexia: Hemodynamics, Blood Volume, Serum Dopamine-?-Hydroxylase Activity, and Arterial Prostaglandin PGE2.- Section Four: Bone Mineral and Matrix Changes Following Spinal Cord Injury: Possible Modes of Treatment.- 13. Disodium Etidronate in the Prevention of Postoperative Recurrence of Heterotopic Ossification in Spinal Cord Injured Patients.- 14. Reversal by Thyrocalcitonin of Depressed Calcium, Magnesium, and Phosphorus Balances in Paraplegic Rats.- 15. Mineral Metabolism and the Effect of Thyrocalcitonin on Periarticular Bone in Spinal Cord Injured Man.- 16. Urinary Excretion of Collagen Metabolites by Quadriplegic Patients.- Section Five: Renal and Urinary Bladder Physiology.- 17. Electromyography of the Human Urinary Bladder.- 18. Effects of Head-Up Tilt on Glomerular Filtration Rate and Renal Plasma Flow in Spinal Man.- Section Six: Hormonal and Behavioral Aspects of Spinal Cord Injury.- 19. Pituitary-Testicular Axis Dysfunction in Spinal Cord Injury.- 20. Psychosexual Adjustment to Spinal Cord Injury — An Holistic Approach.