Clinical neuroscience (New York, N.Y.)最新文献

Although abortive treatment and nonpharmacologic interventions are effective for many if not most patients' occasional migraine attacks, patients who have frequent and/or severe attacks may benefit from preventive pharmacotherapy. This is particularly critical for those patients whose migraines are not treated effectively by acute-care medications because lack of pain control may lead to overuse syndromes that complicate further treatment. Inappropriate use of acute-care medication may contribute to chronic daily headache, tolerance to symptomatic medication, and headache refractory to all treatment. In addition, patients who increase use of acute-care medication due to lack of effect may suffer ergotism, GI problems, liver toxicity, analgesic nephropathy, drug induced-headache, and withdrawal symptoms when overused agents are withdrawn. Finally, overuse of acute-care medication may interfere with the effectiveness of preventive medication. The remainder of this article will focus on when to treat with preventive medication and which medications are currently available for prevention of migraine.

Parkinson's disease (PD) is a major neurologic disorder that distinctively and selectively affects movement and--by extension--the motor system. A large body of evidence has been accumulated over the years showing that movement disorders of PD are also due to sensory disturbances that affect sensorimotor integration. The aim of this review is to discuss the possible contribution of neurophysiologic techniques in evaluating the functionality of sensorimotor integration mechanisms in PD. Somatosensory evoked potentials (SEPs) are an appropriate functional approach for the evaluation of sensory processes in the human brain. SEPs from the frontal scalp sites are considered markers of the functionality of a cortico-subcortico-cortical loop that includes the basal ganglia as well as the premotor and supplementary motor areas. Over the years, it has been demonstrated that PD patients--especially in the early stages of the disease--show a severely depressed frontal responsiveness to sensory stimuli as tested via SEPs. The transient recovery of frontal SEP amplitude after apomorphine, a potent dopamine agonist drug, is a good and specific predictor of the clinical response of PD patients to L-dopa therapy.

The olfactory system is one of the nonmotor systems severely affected in Parkinson's disease (PD). Olfactory dysfunction occurs early in the disease process, is independent of disease stage, duration, and treatment. However, olfactory dysfunction appears to be dependent on disease subtype. Olfaction is mildly impaired or preserved in most of the parkinsonism-plus syndromes (PPS). This provides a means of differential diagnosis between typical PD and PPS. Olfactory function is impaired also in familial forms of parkinsonism in which the genetic defect is known. In familial parkinsonism, olfactory function is impaired in both typical PD and PPS phenotypes. Olfactory dysfunction does not appear to be a manifestation of dopamine deficiency. Olfactory dysfunction is also associated with other neurodegenerative diseases such as Alzheimer's disease (AD), Huntington's disease (HD), as well as with normal aging. The neuropathological changes observed in the olfactory system in PD and other neurodegenerative diseases appear to be disease-specific, raising the possibility that olfactory dysfunction may be the result of a central rather than a peripheral process. The cellular and molecular mechanisms underlying olfactory dysfunction in PD and other neurodegenerative diseases remain unknown.

Magnetic resonance angiography (MRA) refers to a collection of imaging techniques which accentuate the signal intensity of flowing blood and suppress the signal intensity of stationary tissues. The resulting images are processed to resemble conventional catheter angiograms but carry fundamentally different information which is derived from flow rather than anatomy. All MRA techniques are subject to a variety of artifacts can stimulate pathology. A knowledge of the techniques used to produce and display MR angiographic images is essential for their accurate interpretation.

Functional defects of glaucomatous optic neuropathy are reviewed and summarized. Glaucomatous visual field defects are basically comprised of four major patterns: an isolated scotoma, an arcuate scotoma, a nasal step, and generalized depression. The field loss progresses conforming to the optic nerve head and retinal nerve fiber changes. Interpretation of the visual field and some tips of the interpretation are outlined in addition to describing differential diagnosis. Lastly, blue-on-yellow perimetry and high-pass resolution perimetry, both of which are promising tools for early detection of glaucoma, are introduced.

Anterior ischemic optic neuropathy is the most common cause of persistent monocular visual loss in persons over the age of 50. At the heart of this form of optic neuropathy is a sequence of cytoplasmic and membrane events that culminate in axonal destruction. Early depletion of ATP is followed by membrane depolarization, influx of Na+ and Ca2+ via specific voltage-gated channels and reverse operation of the Na+/Ca2+ exchange protein. Toxic Ca2+ overload is the ultimate consequence of these events. Preventing or modulating any of these well-defined steps mitigates against the development of anoxic injury. Translating these molecular insights about how optic nerve axons are damaged by ischemia-like conditions into clinical gains remains the challenge for the future.

Abnormalities of central afferent and efferent pathways have been revealed by evoked potential studies in diabetic patients. Central conduction time is only slightly prolonged; in afferent pathways the primary sensory neuron is more affected than in the subsequent stages, probably as an expression of a central-peripheral distal axonopathy. Central nervous system abnormalities are more frequent in patients with peripheral neuropathy, but evoked potential can be abnormal even in patients without neuropathy. Brainstem auditory evoked potential (BAEP), somatosensory evoked potentials (SEPs) and visual evoked potentials (VEPs) can be affected together, but isolated abnormalities are more frequently observed. Diffuse neuropathological changes have been found in the optic nerves, periventricular regions, brainstem and spinal cord in postmortem pathological studies. Similar changes have been found in animals with experimental diabetes. The pathophysiology of central nervous system (CNS) abnormalities is uncertain, many causes are probably active in including neural damage: chronic hyperglycemia, hypoglycemic episodes, angiopathy, blood-brain barrier dysfunction and others, still unknown.

A multiplicity of peripheral nerve syndromes may develop in patients with diabetes mellitus, the commonest of which is a chronic symmetric sensory polyneuropathy, often associated with autonomic neuropathy. Once established, it is largely irreversible. Acute painful diabetic sensory neuropathy is a separate entity with a favorable prognosis. It now seems likely that chronic inflammatory demyelinating polyneuropathy occurs with greater frequency in diabetic subjects than in the general population and is one explanation for the occurrence of a predominantly motor polyneuropathy. Focal and multifocal peripheral nerve lesions are seen mainly in older diabetic patients and comprise cranial, thoracoabdominal and limb nerve lesions, the last including proximal lower limb diabetic motor neuropathy (diabetic amyotrophy). With this wide array of disorders and the frequency of diabetes, it is important to distinguish those that are directly or indirectly related to diabetes from those that have a coincidental relationship.

Anxiety disorders have a peak age of onset in early adulthood and their prevalence and incidence decline in later life. Most cases of anxiety disorder in late life are chronic, having persisted from younger years. Generalized anxiety and agoraphobia account for most cases of late-onset anxiety. Late-onset generalized anxiety is usually associated with a depressive illness. On the other hand, most individuals with late-onset agoraphobia do not have comorbid depression or a history of panic attacks, and the illness often starts after a traumatic event. Case reports and uncontrolled trials indicate that older persons with anxiety disorders can respond to the same treatments that have been found to be efficacious in younger patients, although it is unknown whether the two groups have similar rates of response. The current clinical reality is that most cases of anxiety disorder in late life are undetected and, when treatment is given, benzodiazepines are overused and antidepressants and behavioral treatments are underused. The high rate of comorbidity between late-onset generalized anxiety and depression in old age suggests that antidepressant medication, rather than benzodiazepines, should be the treatment of choice for this condition.

Neurophysiological studies of language processing in the intact brain have identified 3 major event-related potential (ERP) components correlating with different aspects of language: (1) an early left anterior negativity (ELAN) obtained in correlation with early syntactic processes, primarily processes of structuring the language input, (2) a centroparietal negativity around 400 ms (N400) reflecting lexicalsemantic integration processes, and (3) a late centroparietal positivity (P600) observed in correlation with secondary syntactic processes such as reanalysis and repair. These components manifest themselves approximately around 200 ms, 400 ms and 600 ms post onset of a critical word. Their variation in latency and magnitude can be used as a diagnostic criterion for language impairment.