Journal of neurology
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Complex regional pain syndrome (CRPS) may develop after limb trauma and is characterized by pain, sensory-motor and autonomic symptoms. Most important for the understanding of the pathophysiology of CRPS are recent results of neurophysiological research. Major mechanism for CRPS symptoms, which might be present subsequently or in parallel during the course of CRPS, are trauma-related cytokine release, exaggerated neurogenic inflammation, sympathetically maintained pain and cortical reorganisation in response to chronic pain (neuroplasticity). The recognition of these mechanisms in individual CRPS patients is the prerequisite for a mechanism-oriented treatment.
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The significance of deja vu is widely recognised in the context of temporal lobe epilepsy, and enquiry about deja vu is frequently made in the clinical assessment of patients with possible epilepsy. Deja vu has also been associated with several psychiatric disorders. The historical context of current understanding of deja vu is discussed. ⋯ Several neuroanatomical and psychological models of the deja vu experience are highlighted, implicating the perceptual, mnemonic and affective regions of the lateral temporal cortex, hippocampus and amygdala in the genesis of deja vu. A possible genetic basis for a neurochemical model of deja vu is discussed. Clinical approaches to the patient presenting with possible deja vu are proposed.
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Journal of neurology · Sep 2004
ReviewOptimising MS disease-modifying therapies: antibodies in perspective.
A proportion of people with multiple sclerosis (MS) treated with interferon (IFN) a develop neutralising anti-IFN beta antibodies (NABs). The immunogenicity of the available commercial compounds relates to the genetic structure of the IFN beta molecule, its mode of production, glycosylation status, aggregate formation, commercial formulation, potency, dose, frequency and, possibly, route of administration. At present, it is not possible to predict who will develop NABs usually appear within the first 2 years of starting therapy. ⋯ One could argue that when comparing the 'true' clinical efficacy of different IFN beta products, the comparisons should be limited to the cohorts that remain NAB-negative. As a corollary, the therapeutic efficacy of IFN beta could be maximised if patients who tolerate higher-dose preparations could be prevented from developing persistent NABs. Strategies employed to prevent or reverse the development of NABs with other biological compounds (e. g. insulin, factor VIII, IFN beta, recombinant human erythropoietin) include improvements in the manufacturing process, immunosuppression, induction of tolerance and deimmunisation, and these should be considered in relation to biological DMT therapy as part of future clinical studies.
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Journal of neurology · Jun 2004
ReviewTrigeminocardiac reflex. A clinical phenomenon or a new physiological entity?
The trigemino-cardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea or gastric hypermotility during stimulation of any of the sensory branches of the trigeminal nerve. The sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. This afferent pathway continues along the short internuncial nerve fibers in the reticular formatio to connect with the efferent pathway in the motor nucleus of the vagus nerve. ⋯ By this physiological response, the adjustments of the systemic and cerebral circulations are initiated to divert blood to the brain or to increase blood flow within it. As it is generally accepted that the diving reflex and ischemic tolerance appear to involve at least partially similar physiological mechanisms, the existence of such endogenous neuroprotective strategies may extend the actually known clinical appearance of the TCR and include the prevention of other potentially brain injury states as well. This may be in line with the suggestion that the TCR is a physiological, but not a pathophysiological entity.
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Journal of neurology · Feb 2004
ReviewBotulinum toxin in the treatment of rare head and neck pain syndromes: a systematic review of the literature.
Botulinum neurotoxin (BoNT) is used to treat various neurological disorders associated with pathologically increased muscle tone. Botulinum toxin inhibits the release of the neurotransmitter acetylcholine at the neuromuscular junction thereby inhibiting striatal muscle contractions. Besides the reduction in muscle tone BoNT tends to reduce pain in pain syndromes associated with muscle spasm. In addition, BoNT has been proposed as an analgesic, suggesting alternative non-cholinergic mechanisms of action.Surprisingly, BoNT was reported as a potential treatment for tension-type headache and migraine-both primary headache syndromes without an apparent muscular component-however, varying responses to BoNT have been found, overall without sufficient evidence for a general treatment. In this systematic review we set out to clarify the efficacy and safety of BoNT in the treatment of rare head and neck pain syndromes (e. g. cervicogenic headache, chronic paroxysmal hemicrania, cluster headache, trigeminal neuralgia, temporomandibular disorders, cervical dystonia and whiplash injuries). ⋯ There is convincing evidence for the effectiveness of BoNT in the treatment of pain associated with cervical dystonia. Due to the frequent adverse effects predominantly observed with higher doses, the trade off in risk and benefit should be carefully considered in each case. For all other rare head and neck pain syndromes we found no RCTs (cluster headache, chronic paroxysmal hemicrania, trigeminal neuralgia) and only a few small sized trials (cervicogenic headache, chronic neck pain, temporomandibular disorders). We were therefore unable to draw any definite conclusions.