Handbook of clinical neurology
-
There is an increasing incidence and prevalence of patients with chronic kidney disease (CKD) in Western industrialized countries and currently is estimated at approximately 10% of adults aged over 20 years. Renal failure causes an excessively increased risk of cerebrovascular and cardiovascular complications. Moreover, renal failure leads to a number of the neurologic symptoms neurologists are often confronted with. ⋯ Complications of the central nervous system (e.g., uremic encephalopathy, disequilibrium syndrome, and drug induced disorders) are reviewed. It has long been known that uremia leads to peripheral nerve injury. Frequent neurological diseases such as uremic polyneuropathy, autonomic neuropathy, and a range of mononeuropathies are discussed.
-
Cardiac transplantation remains the best treatment option for patients with end-stage, NYHA class IV heart failure who have failed conventional therapy. However, transplant rates have remained static largely due to limited organ donor supplies. Therefore, appropriate allocation of this precious resource is critical to maximize benefit, both at a patient level and at a societal level. ⋯ These include: (1) drug toxicities, such as lowering of seizure thresholds; (2) encephalopathy, such as posterior reversible encephalopathy syndrome (PRES); (3) infections; (4) malignancies, such as post-transplant lymphoproliferative disorder (PTLD). Many of the same considerations discussed in adult heart transplant recipients apply to pediatric heart transplant recipients as well. In children, seizures are the most common neurologic complication, although other neurologic complication rates are comparable.
-
Patients with hemophilia and other congenital bleeding disorders are at risk for development of central nervous system (CNS) hemorrhage and can present with acute or chronic neurologic symptoms. These disorders are generally caused by qualitative or quantitative deficiency of components of hemostasis such as coagulation proteins, von Willebrand factor, or platelets. ⋯ Since hemophilia is the most common bleeding disorder encountered in clinical practice, more emphasis is placed on management of hemophilia. Additionally, neurologic manifestations related to the bleeding diathesis in patients with hemophilia are elaborated.
-
Syncope describes a sudden and brief transient loss of consciousness (TLOC) with postural failure due to cerebral global hypoperfusion. The term TLOC is used when the cause is either unrelated to cerebral hypoperfusion or is unknown. The most common causes of syncopal TLOC include: (1) cardiogenic syncope (cardiac arrhythmias, structural cardiac diseases, others); (2) orthostatic hypotension (due to drugs, hypovolemia, primary or secondary autonomic failure, others); (3) neurally mediated syncope (cardioinhibitory, vasodepressor, and mixed forms). ⋯ Basic diagnostic workup of TLOC includes a thorough history and physical examination, and a 12-lead electrocardiogram (ECG). Blood testing, electroencephalogram (EEG), magnetic resonance imaging (MRI) of the brain, echocardiography, head-up tilt test, carotid sinus massage, Holter monitoring, and loop recorders should be obtained only in specific contexts. Management strategies involve pharmacologic and nonpharmacologic interventions, and cardiac pacing.
-
Complex multiorgan failure may require simultaneous transplantation of several organs, including heart-lung, kidney-pancreas, or multivisceral transplantation. Solid organ transplantation can also be combined with hematopoietic stem cell transplantation to modulate immunologic response to a solid organ allograft. Combined multiorgan transplantation may offer a lower rate of allograft rejection and lower immunosuppression needs. ⋯ Heart-lung allograft recipients have very similar clinical course and spectrum of neurologic complications to lung transplant recipients. At this time there are no reports of an increased risk of graft-versus-host disease with combined transplantation of solid organ allograft and hematopoietic stem cells. Chronic immunosuppression and complex toxic-metabolic disturbances after multiorgan transplantation create a permissive environment for development of a wide spectrum of neurologic complications which largely resemble complications after transplantations of individual components of complex multiorgan allografts.