Handbook of clinical neurology
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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.
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Painful diabetic distal symmetrical polyneuropathy (painful DPN) is a puzzle with two important missing pieces: Firstly we still do not understand why only some patients with neuropathy experience painful symptoms; Secondly we still do not have a complete understanding of how nociception generated in the peripheral nervous system is processed by the central nervous system (CNS). Available treatments offer only symptom relief and there is currently no effective treatment based on arresting or reversing the progression of disease. Therefore the management of painful DPN remains less than optimal because the complex pathophysiology of nociception and pain perception in health and disease is incompletely understood. ⋯ Combining the knowledge from these two streams of enquiry we will soon be able to predict accurately who will develop painful DPN, how we can halt or reverse the condition, or who will respond to symptomatic treatments. Future developments in the treatment of painful DPN will be underpinned by decoding the peripheral and central mechanisms of pain. Research is focusing on these areas of enquiry in the hope that answers will lead to effective treatments to alleviate pain and reverse pathology for those suffering from painful DPN.
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Alcoholism, more generically drug addiction, can be defined as a chronically relapsing disorder characterized by: (1) compulsion to seek and take the drug (alcohol); (2) loss of control in limiting (alcohol) intake; and (3) emergence of a negative emotional state (e.g., dysphoria, anxiety, irritability), reflecting a motivational withdrawal syndrome, when access to the drug (alcohol) is prevented (defined here as dependence). The compulsive drug seeking associated with alcoholism can be derived from multiple neuroadaptations, but the thesis argued here, derived largely from animal models, is that a key component involves decreased brain reward function, increased brain stress function, and compromised executive function, all of which contribute to the construct of negative reinforcement. Negative reinforcement is defined as drug taking that alleviates a negative emotional state. ⋯ A brain stress response system is hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence, and to contribute to the compulsivity of alcoholism. Other components of brain stress systems in the extended amygdala that interact with CRF and may contribute to the negative motivational state of withdrawal include increases in norepinephrine function, increases in dynorphin activity, and decreases in neuropeptide Y. The combination of impairment of function in reward circuitry and recruitment of brain stress system circuitry provides a powerful neurochemical basis for the negative emotional states that are responsible for the negative reinforcement that drives the compulsivity of alcoholism.
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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.
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Independent of the underlying condition, critical illness is characterized by a uniform dysregulation of the hypothalamic-pituitary-peripheral axes. In most axes a clear biphasic pattern can be distinguished. The acute phase of critical illness is characterized by low peripheral effector hormone levels such as T3, IGF-1 and testosterone, despite an actively secreting pituitary. ⋯ In the prolonged phase of critical illness, low peripheral effector hormone levels coincide with a uniform suppression of the neuroendocrine axes, predominantly of hypothalamic origin. The severity of the alterations in the different neuroendocrine axes is associated with a high risk of morbidity and mortality, but it remains unknown whether the observed changes are cause or consequence of adverse outcome. Several studies have identified therapeutic potential of hypothalamic releasing factors, but clinical outcome remains to be investigated with sufficiently powered randomized controlled trials.