Search

An acute reduction in plasma osmolality causes rapid uptake of water by astrocytes but not by neurons, whereas both cell types swell as a consequence of lost blood flow (ischemia). Either hypoosmolality or ischemia can displace the brain downwards, potentially causing death. However, these disorders are fundamentally different at the cellular level. Astrocytes osmotically swell or shrink because they express functional water channels (aquaporins), whereas neurons lack functional aquaporins and thus maintain their volume. Yet both neurons and astrocytes immediately swell when blood flow to the brain is compromised (cytotoxic edema) as following stroke onset, sudden cardiac arrest, or traumatic brain injury. In each situation, neuronal swelling is the direct result of spreading depolarization (SD) generated when the ATP-dependent sodium/potassium ATPase (the Na+/K+ pump) is compromised. The simple, and incorrect, textbook explanation for neuronal swelling is that increased Na+ influx passively draws Cl− into the cell, with water following by osmosis via some unknown conduit. We first review the strong evidence that mammalian neurons resist volume change during acute osmotic stress. We then contrast this with their dramatic swelling during ischemia. Counter-intuitively, recent research argues that ischemic swelling of neurons is non-osmotic, involving ion/water cotransporters as well as at least one known amino acid water pump. While incompletely understood, these mechanisms argue against the dogma that neuronal swelling involves water uptake driven by an osmotic gradient with aquaporins as the conduit. Promoting clinical recovery from neuronal cytotoxic edema evoked by spreading depolarizations requires a far better understanding of molecular water pumps and ion/water cotransporters that act to rebalance water shifts during brain ischemia.

Guillain-Barré syndrome (GBS), when severe, involves the autonomic nervous system; our objective was to assess the spectrum and predictors of dysautonomia, and how it may impact functional outcomes.A retrospective review of patients admitted to the Mayo Clinic in Rochester, MN between January 1, 2000, and December 31, 2017, with GBS and dysautonomia was performed. Demographics, comorbidities, parameters of dysautonomia, clinical course, GBS disability score, and Erasmus GBS Outcome Score (EGOS) at discharge were recorded.One hundred eighty seven patients were included with 71 (38%) noted to have at least one manifestation of dysautonomia. There are 72% of patients with a demyelinating form of GBS and 36% of patients with demyelination had dysautonomia. Ileus (42%), hypertension (39%), hypotension (37%), fever (29%), tachycardia or bradycardia (27%), and urinary retention (24%) were the most common features. Quadriparesis, bulbar and neck flexor weakness, and mechanical ventilation were associated with autonomic dysfunction. Patients with dysautonomia more commonly had cardiogenic complications, syndrome of inappropriate antidiuretic hormone, posterior reversible encephalopathy syndrome, and higher GBS disability score and EGOS. Mortality was 6% in patients with dysautonomia versus 2% in the entire cohort (P = 0.02).Dysautonomia in GBS is a manifestation of more severe involvement of the peripheral nervous system. Accordingly, mortality and functional outcomes are worse. There is a need to investigate if more aggressive treatment is warranted in this category of GBS.

Hyponatremia, defined as a serum sodium concentration ([Na+]) less than 135 mEq/L, is commonly caused by elevated levels of the hormone arginine vasopressin (AVP), which causes water retention. The principal organ affected by disease-related morbidity is the brain. The neurologic complications associated with hyponatremia are attributable to cerebral edema and increased intracranial pressure, caused by the osmotically driven movement of water from the extracellular compartment into brain cells. Although neurologic symptoms induced by hyponatremia are limited by an adaptive brain mechanism known as "regulatory volume decrease," an overly rapid correction of serum [Na+] before the reversal of this adaptive response can also produce neurologic damage. The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hyponatremia related to central nervous system disorders, neurosurgery, or the use of psychoactive drugs. Fluid restriction is the standard of care for patients with SIADH who are asymptomatic or who have only mild symptoms, but patients with severe or symptomatic hyponatremia require more aggressive therapy. Infusion of hypertonic saline is the usual approach to the treatment of symptomatic hyponatremia, but patients require frequent monitoring. Pharmacologic agents such as demeclocycline and lithium may be effective in some patients but are associated with undesirable adverse events. The AVPreceptor antagonists are a new therapeutic class for the treatment of hyponatremia. The first agent in this class approved for the treatment of euvolemic hyponatremia in hospitalized patients is conivaptan. Two other agents, tolvaptan and lixivaptan, are being evaluated in patients with euvolemic and hypervolemic hyponatremia. The AVP-receptor antagonists block the effects of elevated AVP and promote aquaresis, the electrolyte-sparing excretion of water, resulting in the correction of serum [Na+]. These agents may also have intrinsic neuroprotective effects.

To review histopathological and clinical data linking endocrine failure to traumatic brain injury (TBI) during acute neurosurgical treatment and rehabilitation.A focused search of the Medline (PubMed) medical literature database and the authors' files were used to identify selected publications.Endocrine failure may produce clinically important consequences during acute and convalescent care after TBI, and may be caused by direct injury to the hypothalamic- pituitary axis (HPA), neuroendocrinological effects from catecholamines and cytokines, or from systemic infection/inflammation that produces primary gland failure. Autopsy evidence of hemorrhage or ischemia in the HPA is common soon after TBI. The estimated incidence of acute hormone reduction is adrenal 15%, thyroid 5 - 15%, growth hormone 18%, vasopressin 3 - 37%, and gonadal (25 - 80%). Hyperprolactinemia occurs in more than 50% of patients. Inappropriate secretion of antidiuretic hormone (SIADH) and the euthyroid sick syndrome are common. Acute adrenal failure, central hypothyroidism, SIADH, and diabetes insipidus (DI) may cause poor neurological outcomes including death, hypo/hypernatremia, hypotension, and increased vasoactive drug requirements. Treatment of those conditions is warranted. Delayed diagnosis of hypopituitarism is often mistaken for symptoms of residual head injury. Some chronic hormone deficiency occurs in 30 - 40% of selected patients after TBI, more than one deficiency in 10 - 15%, growth hormone in 15 - 20%, gonadal hormones in 15%, and hypothyroidism in 10 - 30%. Chronic adrenal failure and DI are reported over a wide incidence. Prolactin is elevated in 30%. All clinical symptoms respond favorably to replacement therapy.Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.

Hyponatremia is common in neurocritical care patients and is associated with significant morbidity and mortality. Despite decades of research into the syndrome of inappropriate antidiuretic hormone (SIADH) and cerebral salt wasting (CSW), their underlying pathophysiological mechanisms are still not fully understood. This paper reviews the history behind our understanding of hyponatremia in patients with neurologic injury, including the first reports of CSW and SIADH, and current and future challenges to diagnosis and management in this setting. Such challenges include distinguishing CSW, SIADH, and hypovolemic hyponatremia due to a normal pressure natriuresis from the administration of large volumes of fluids, and hyponatremia due to certain medications used in the neurocritical care population. Potential treatments for hyponatremia include mineralocorticoids and vasopressin 2 receptor antagonists, but further work is required to validate their usage. Ultimately, a greater understanding of the pathophysiological mechanisms underlining hyponatremia in neurocritical care patients remains our biggest obstacle to optimizing patient outcomes in this challenging population.

Cerebral salt wasting syndrome (CSWS) and the syndrome of inappropriate antidiuretic hormone (SIADH) are both causes of hyponatremia in pediatric neurosurgical patients often with similar presenting symptoms; however, despite similar clinical characteristics the treatment for CSWS and SIADH can be drastically different, which makes the distinction critical for post-operative treatment. Further complicating matters, are the exact mechanism for CSWS which remains unclear, and the incidence and severity of CSWS is not well studied in pediatric neurosurgical patients. We hypothesized that CSWS occurs frequently in post-operative brain tumor patients and is an important cause of post-operative hyponatremia in these patients. We designed a single institution retrospective cohort study of all pediatric brain tumor patients undergoing craniotomy for tumor resection at our institution between January 2005 and December 2009. Of the 282 patients undergoing 291 operations, post-operative CSWS was identified in 15 cases (5%), and was more frequently observed than SIADH (nine cases, 3%). Median onset of CSWS was on post-operative day 3, lasting a median of 2.5 days. Patients with CSWS were more likely to have suffered post-operative stroke (40 vs. 4.6%, P