Seminars in neurology
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Neurologic dysfunction is a common side effect of many chemotherapy drugs. For several agents, neurotoxicity is common, severe, and can be dose-limiting. As the list of newer chemotherapy agents and systemic "targeted therapies" grows, so does the number and variety of potential neurotoxicities. This is a review of the clinical features of chemotherapy-induced syndromes involving the central and peripheral nervous systems.
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Seminars in neurology · Apr 2010
ReviewTrigeminal autonomic cephalalgias: paroxysmal hemicrania, SUNCT/SUNA, and hemicrania continua.
The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders that include cluster headache (CH), paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing/cranial autonomic features (SUNCT/SUNA). Hemicrania continua (HC) is often included with this group, although the second edition of The International Classification of Headache Disorders did not link the entities. Trigeminal autonomic cephalalgias are generally characterized by relatively short-lasting attacks of severe pain and lateralized associated features including the pain, cranial autonomic symptoms, and where present, migrainous symptoms, such as photophobia. ⋯ Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing has the shortest attack duration and the highest attack frequency. Hemicrania continua has a continuous pain with exacerbations that can include cranial autonomic symptoms as part of the phenotype. The syndromes share much in their pathophysiology and investigation paths; however, their treatment is distinct, so that the accurate differentiation is important for optimal management.
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Primary headache disorders encompass a heterogeneous group of neurologic disorders that cause recurrent or persistent head pain without any clear underlying cause. The epidemiology of the most common primary headache disorders, tension-type headache and migraine, the most common trigeminal autonomic cephalalgia, cluster headache, as well as chronic daily headache are addressed in this review. The incidence, prevalence, burden, and comorbidities of these disorders are discussed, and the risk factors for progression from episodic to chronic daily headache are also reviewed.
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Distinguishing primary headache from secondary headache is the first objective of every new clinical encounter with a patient complaining of headache. The history is king in headache medicine-90% of patients presenting with headache have a primary headache disorder and the examination is normal. The history must be elicited because patients will not always volunteer seminal information. ⋯ The second objective, of course, is making the correct diagnosis of the primary headache disorder. Although at first glance this appears obvious and almost patronizing, making the correct diagnosis is often not a priority, nor is it a process that is emphasized in undergraduate and postgraduate training programs. Knowing some simple rules and standard questions will make the process almost fail proof.
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Myasthenia gravis is typically an acquired autoimmune disorder in which antibodies are directed at structural components of the neuromuscular junction, most commonly the nicotinic acetylcholine receptor. The clinical manifestations of skeletal muscle weakness are broad. Patients most often report fatigable muscle weakness. ⋯ Symptoms may be confined to the eyes (ocular myasthenia) or reflect bulbar, limb, or respiratory muscle weakness (generalized myasthenia). The diagnosis is based on a characteristic history and the finding of fatigable muscle weakness on examination, and may be supported by diagnostic tests such as finding elevated titers of acetylcholine receptor or muscle-specific receptor tyrosine kinase (MuSK) antibodies, a positive Tensilon test, a decremental response on slow repetitive nerve stimulation, and abnormal jitter on single fiber electromyography. This article presents a series of pearls to aid in the clinical and laboratory diagnosis of myasthenia gravis, emphasizing key historical features, common and characteristic findings on examination, and potential pitfalls in the use of ancillary diagnostic studies.