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The in vitro autoradiographic distribution of calcium channel antagonist binding sites for 1,4-dihydropyridine and phenylalkylamine has been investigated in rat, guinea pig and human brain. 1,4-dihydropyridine ([3H] (+) PN200-110) and phenylalkylamine ([3H] (-) D-888) binding sites are identically distributed in the brain of the three mammalian species studied. High densities of calcium antagonist binding sites are present in brain areas enriched in synaptic contacts such as the hippocampus, cortex and striatum. Low to moderate densities of sites are found in other regions such as the thalamus, hypothalamus and brain stem. These data demonstrate the existence of specific calcium antagonist binding sites in mammalian brain including man. These sites are discretely distributed with highest concentrations present in the hippocampus and cortex. Moreover, the similar distribution of binding sites for [3H] (+) PN200-110 and [3H] (-) D-188 suggests that 1,4-dihydropyridine and phenylalkylamine bind to the same receptor site complex in mammalian brain.

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The diversity of pathogenetic mechanisms involved in posttraumatic visual impairment was reviewed in a study of the hospital records of 24 patients admitted with multiple injuries. Most major visual abnormalities occurred in young people (average age 33 years) who presented with a wide range of overall severity of injury (injury severity score 13-47) and involvement of the central nervous system (Glasgow coma scale 5-15). Bilateral or monocular blindness developed in 63% of patients. Seventy percent of the injuries involved the anterior visual pathways with damage to the optic nerve alone accounting for 35%. Fractures of the sphenoid bone, particularly of the body, accompanied optic nerve and chiasmal injuries and some cases of traumatic carotid-cavernous fistulas. Pathogenetic mechanisms varied according to the site of injury and included vitreous hemorrhage and optic atrophy secondary to raised intracranial pressure, retinal hypoxia from carotid-cavernous fistulas, shearing and compression injuries of the optic nerve, traumatic chiasmal syndrome, temporoparietal and occipital contusions, and transtentorial herniation with occipital infarction. Visual abnormalities varied in severity from moderately reduced visual acuity and diverse hemianopias and scotomas to blindness. The incidence of posttraumatic residual visual abnormalities is likely to increase in the wake of improved acute care of the traumatized victim.

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Consecutive craniotomies (118) drawn from major hospitals, and performed for disorders other than epilepsy or acute trauma were reviewed. The final diagnosis included tumor (70), subdural hematoma (13), aneurysm (10), arteriovenous malformation (7), and miscellaneous lesions (18). Eighty-seven (73.7%) patients had not experienced seizures prior to neurosurgery, 11 of these (12.6%) had a seizure within the first week, in six the attack occurred within 24 hours, and of these three had further attacks. In contrast, of the 31 patients (26.3%) that had one or more seizures prior to operation, 11 patients (35.5%) had seizures within the first week. In ten patients seizures occurred within the first 24 hours and of these seven had one or more recurrences later in the week. Anticonvulsant drugs were administered to 72 patients before operation, including all those with a history of seizures, but loading doses were not utilized to ensure therapeutic levels. In patients with predisposing factors to postoperative seizures, anticonvulsant drugs should be administered before or immediately following craniotomy in adequate dosage to rapidly achieve and maintain effective plasma levels. Phenytoin, owing to its minimal sedative effects is the drug of choice. A loading dose of 18 milligrams per kilogram can be safely administered as an admixture to an intravenous infusion of 0.9% saline with careful monitoring of cardiopulmonary function.

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It has recently been shown that ice massage of the web between the thumb and index finger produces significantly greater relief of dental pain than a placebo control procedure. These results indicate that ice massage may be comparable to transcutaneous electrical stimulation (TES) and acupuncture, and may be mediated by similar neural mechanisms. The purpose of this study was to examine the relative effectiveness of ice massage and TES for the relief of low-back pain. Patients suffering chronic low-back pain were treated with both ice massage and TES. The order of treatments was balanced, and changes in the intensity of pain were measured with the McGill Pain Questionnaire (MPQ). The results show that both methods are equally effective: based on the Pain Rating Index of the MPQ, 67-69% of patients obtained pain relief greater than 33% with each method. The results indicate that ice massage is an effective therapeutic tool, and appears to be more effective than TES for some patients. It may also serve as an additional sensory-modulation method to alternate with TES to overcome adaptation effects. Evidence that cold signals are transmitted to the spinal cord exclusively by A-delta fibers and not by C fibers suggests that ice massage provides a potential method for differentiating among the multiple feedback systems that mediate analgesia produced by different forms of intense sensory input.

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