Annals of neurology
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Annals of neurology · Jul 2005
Comparative StudyDepth of delayed cooling alters neuroprotection pattern after hypoxia-ischemia.
Hypothermia after perinatal hypoxia-ischemia (HI) is neuroprotective; the precise brain temperature that provides optimal protection is unknown. To assess the pattern of brain injury with 3 different rectal temperatures, we randomized 42 newborn piglets: (Group i) sham-normothermia (38.5-39 degrees C); (Group ii) sham-33 degrees C; (Group iii) HI-normothermia; (Group iv) HI-35 degrees C; and (Group v) HI-33 degrees C. Groups iii through v were subjected to transient HI insult. ⋯ Comparing hypothermia at 35 and 33 degrees C, 35 degrees C resulted in more viable neurons in deep GM, whereas 33 degrees C resulted in more viable neurons in cortical GM (both p < 0.05). These results suggest that optimal neuroprotection by delayed hypothermia may occur at different temperatures in the cortical and deep GM. To obtain maximum benefit, you may need to design patient-specific hypothermia protocols by combining systemic and selective cooling.
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Annals of neurology · Jun 2005
Erythromelalgia: a hereditary pain syndrome enters the molecular era.
In contrast with acquired pain syndromes, molecular substrates for hereditary pain disorders have been poorly understood. Familial erythromelalgia (Weir Mitchell's disease), also known as primary erythermalgia, is an autosomal dominant disorder characterized by burning pain in the extremities in response to warm stimuli or moderate exercise. The cause of this disorder has been enigmatic, and treatment has been empirical and not very effective. ⋯ Erythromelalgia is the first human disorder in which it has been possible to associate an ion channel mutation with chronic neuropathic pain. Identification of mutations within a peripheral neuron-specific sodium channel suggests the possibility of rational therapies that target the affected channel. Moreover, because some other pain syndromes, including acquired disorders, involve altered sodium channel function, erythromelalgia may emerge as a model disease that holds more general lessons about the molecular neurobiology of chronic pain.
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The rare primary headache short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is characterized by 3 to 200 attacks per day of severe unilateral orbital pain. Functional magnetic resonance imaging shows increased blood flow in the ipsilateral posterior inferior hypothalamus during attacks, indicating activation. We report the first patient with SUNCT in whom severe intractable pain (70 per day) was well controlled by electrode implant to and continuous stimulation of the posterior inferior hypothalamus. Ann Neurol 2005;57:925-927.
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Annals of neurology · Jun 2005
Gene transfer of glutamic acid decarboxylase reduces neuropathic pain.
We tested whether transfer of the gene coding for glutamic acid decarboxylase to dorsal root ganglion using a herpes simplex virus vector to achieve release of GABA in dorsal horn would attenuate nociception in this condition. Subcutaneous inoculation of a replication-defective herpes simplex virus vector expressing glutamic acid decarboxylase (vector QHGAD67) 7 days after selective L5 spinal nerve ligation reversed mechanical allodynia and thermal hyperalgesia; the antiallodynic effect lasted 6 weeks and was reestablished by reinoculation. QHGAD67 inoculation also suppressed induction of c-Fos and phosphorylated extracellular signal-regulated kinase 1 and 2 in the spinal cord.
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Annals of neurology · May 2005
ReviewNeurocognitive complications after coronary artery bypass surgery.
Both short- and long-term cognitive changes continue to occur after coronary artery bypass grafting (CABG), but the pathophysiology of these neurobehavioral changes remains incompletely understood. The persistence of mild postoperative neurocognitive changes despite multiple improvements in the cardiopulmonary bypass procedure may be partially because of surgical populations being older and having more prevalent comorbid disease. The cause of the early postoperative changes is most likely multifactorial and may include ischemic injury from microemboli, hypoperfusion, and other factors resulting from major surgery. ⋯ A history of hypertension and other risk factors for vascular disease is known to be associated with increased risk for long-term cognitive decline in community-dwelling elderly individuals. Cerebrovascular risk factors are also associated with silent magnetic resonance imaging abnormalities in patients undergoing CABG. Thus, whereas both short- and long-term postoperative cognitive changes have been associated with CABG, only the short-term, transient changes appear to be directly related to the use of cardiopulmonary bypass.