To obtain an estimate of how often practicing neurologists in California encounter unexpected strokes, myelopathies, or radiculopathies following chiropractic manipulation, we surveyed each member of the American Academy of Neurology in California and inquired about the number of patients evaluated over the preceding 2 years who suffered a neurologic complication within 24 hours of chiropractic manipulation. Four hundred eighty-six neurologists were surveyed, 177 responded; 55 strokes, 16 myelopathies, and 30 radiculopathies were reported. Patients were between the ages of 21 and 60, and the majority experienced complications following cervical manipulation. Most of the patients continued to have persistent neurologic deficits 3 months after the onset, and about one-half had marked or severe deficits. Nearly all of the strokes involved the posterior circulation and almost one-half were angiographically proven. Patients, physicians, and chiropractors should be aware of the risk of neurologic complications associated with chiropractic manipulation.
Induction of stroke not only produces local ischemia and brain damage, but also has profound effects on peripheral immune responses. In the current study, we evaluated effects on spleen and blood cells 4 days after stroke induction. Surprisingly, there was a less inflammatory cytokine profile in the middle cerebral artery occlusion-affected right brain hemisphere at 96 h compared with earlier time points. Moreover, our results demonstrate that stroke leads to splenic atrophy characterized by a reduction in organ size, a drastic loss of splenocyte numbers, and induction of annexin V + and TUNEL + cells within the spleen that are in the late stages of apoptosis. The consequence of this process was to reduce T cell proliferation responses and secretion of inflammatory cytokines, resulting in a state of profound immunosuppression. These changes produced a drastic reduction in B cell numbers in spleen and blood, and a novel increase in CD4 + FoxP3 + regulatory T cells. Moreover, we detected a striking increase in the percentage of nonapoptotic CD11b + VLA-4-negative macrophages/monocytes in blood. Immunosuppression in response to brain injury may account for the reduction of inflammatory factors in the stroke-affected brain, but also potentially could curtail protective immune responses in the periphery. These findings provide new evidence to support the contention that damage to the brain caused by cerebral ischemia provides a powerful negative signal to the peripheral immune system that ultimately induces a drastic state of immunosuppression caused by cell death as well as an increased presence of CD4 + FoxP3 + regulatory T cells.Induction of inflammatory factors clearly contributes to postocclusion damage in strokeinjured brain tissue (1,2). Damage sustained by the brain during stroke also results in rapid systemic changes in inflammatory cells, cytokines, and chemokines in the circulation and peripheral immune organs. In patients with stroke, C-reactive protein, white blood cell counts, and plasma IL-6 levels were increased on admission and persisted for >7 days (3). A later study NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript from this group found a significant correlation in peak plasma IL-6 levels measured within the first week after the stroke with brain infarct volume, stoke severity, and long-term clinical outcome (4). Additionally, experimental stroke in mice caused a reduction in immune cells in peripheral lymphoid organs and decreased secretion of TNF-α and IFN-γ that contributed to spontaneous bacterial infections, a leading cause of mortality in stroke patients (5). Moreover, occlusion of the left or right hemispheres in rats caused a transient reduction in total splenocytes and CD8 + T cells, and increased splenocyte proliferation to mitogens (6).In a recent report (7), we confirmed elevated plasma IL-6 levels in middle cerebral artery occlusion (MCAO) 3 mice through 22 h after occlusion, as well as increased IFN-γ and MCP-1 at the 6 h time point. Moreover, we obser...
Analysis of neural activity-dependent fluctuations in K+, H+, and ECS dimensions in the developing RON has revealed major changes during the first two to three postnatal weeks. The emergence of the adult ceiling level for evoked extracellular K+ (10 to 12 mM) and significant ECS shrinkage are roughly correlated in time with the proliferation and maturation of glial cells in this structure. This observation and others have led to the hypothesis that ECS shrinkage depends upon electrolyte and water transport into glial cells with subsequent swelling. Development of the adult K+ ceiling level may also depend upon glial cells, but it is likely that other factors contribute to this homeostatic mechanism. Marked alterations in activity-dependent pHo shifts were seen with development and may be related to changes in the activity of carbonic anhydrase in this structure. The technological means are at hand to pursue these questions vigorously in an effort to provide further insight into the mechanisms of ionic and fluid homeostasis of brain ECS, and the developing RON appears to be a useful model system in this regard.
In gray matter (GM), anoxia induces prominent extracellular ionic changes that are important in understanding the pathophysiology of this insult. White matter (WM) is also injured by anoxia but the accompanying changes in extracellular ions have not been studied. To provide such information, the time course and magnitude of anoxia-induced changes in extracellular K+ concentration ([K+]o) and extracellular pH (pHo) were measured in the isolated rat optic nerve, a representative central WM tract, using ion-selective microelectrodes. Anoxia produced less extreme changes in [K+]o and pHo in WM than are known to occur in GM; in WM during anoxia, the average maximum [K+]o was 14 +/- 2.9 mM (bath [K+]o = 3 mM) and the average maximum acid shift was 0.31 +/- 0.07 pH unit. The extracellular space volume rapidly decreased by approximately 20% during anoxia. Excitability of the rat optic nerve, monitored as the amplitude of the supramaximal compound action potential, was lost in close temporal association with the increase in [K+]o. Increasing the bath glucose concentration from 10 to 20 mM resulted in a much larger acid shift during anoxia (0.58 +/- 0.08 pH unit) and a smaller average increase in [K]o (9.2 +/- 2.6 mM). The increased extracellular glucose concentration presumably provided more substrate for anaerobic metabolism, resulting in more extracellular lactate accumulation (although not directly measured) and a greater acid shift. Enhanced anaerobic metabolism during anoxia would provide energy for operation of ion pumps, including the sodium pump, that would result in smaller changes in [K+]o. These effects were probably responsible for the observation that the optic nerve showed significantly less damage after 60 min of anoxia in the presence of 20 mM glucose compared to 10 mM glucose. Under normoxic conditions, increasing bath K+ concentration to 30 mM (i.e., well beyond the level shown to occur with anoxia) for 60 min caused abrupt loss of excitability during the period of application but minimal change in the amplitude of the compound action potential following the period of exposure. The anoxia-induced increase in [K+]o, therefore, was not itself directly responsible for irreversible loss of optic nerve function. These observations indicate that major qualitative differences exist between mammalian GM and WM with regard to anoxia-induced extracellular ionic changes.
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