Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Cranial neuralgias are paroxysmal painful disorders of the head characterised by some shared features such as unilaterality of symptoms, transience and recurrence of attacks, superficial and "shock-like" quality of pain and the presence of triggering factors. Although rare, these disorders must be promptly recognised as they harbour a relatively high risk for underlying compressive or inflammatory disease. ⋯ If the aetiology of trigeminal neuralgia (TN) and other typical neuralgias must be brought back to the peripheral injury, their pathogenesis could involve central allodynic mechanisms, which, in patients with inter-critical pain, also engage the nociceptive neurons at the thalamic-cortical level. Currently available medical treatments for TN and other cranial neuralgias are reviewed.
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Chronic daily headache that does not respond or no longer responds to prophylaxis is commonly encountered at specialist headache centres. Animal and brain imaging studies indicate that peripheral neurostimulation affects brain areas involved in pain modulation, providing a rationale for its use in these conditions. We examine problems related to the selection of chronic daily headache patients for peripheral neurostimulation. ⋯ These considerations suggest the need for extensive characterisation of patients proposed for neurostimulation. We propose that patients being considered for neurostimulation should be followed for at least a year, and that their headache over this time should consistently be frequent (all or most days) and drug refractory. We also propose that only completely drug-resistant (as opposed to partially drug-resistant) patients be considered for neurostimulation unless there are other indications.
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Improvement in the biomedical and biotechnological research fields have allowed refinement of the neuromodulation approach in the treatment of a subgroup of medical disorders otherwise refractory to pharmacological treatment, such as chronic primary headaches. Chronic pain conditions imply central sensitisations and functional reorganisation that cannot be quickly or easily reversed. It appears evident that conventional treatment can sometimes be unsuccessful or only partially successful, and that relapse is common. ⋯ In 2000 these findings prompted a functional neurosurgery approach, with the first case of deep brain hypothalamic stimulation (DBS) in a severely disabled chronic CH patient. Since then, 18 implants in our centre and many others in different countries have been performed. Although the outcomes are encouraging, the invasive nature of the technique and the occurrence of rare but major adverse events have suggested a safer peripheral approach with occipital nerve stimulation (ONS).
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The role of psychological factors related to headache, particularly tension-type headache (TTH), has long been a focus of investigation. The subject at issue is a complex one, with some aspects that are still being debated by experts. In episodic TTH, it is possible to hypothesise that headache is not only a "primary" headache that causes gratuitous pain to sufferers. ⋯ These findings suggest that people with TTH may have difficulty in expressing their emotions. Finally, psychological factors and emotional disturbances have been indicated as risk factors for TTH. Indeed, stress and mental tension are the most common factors that cause TTH.
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Migraine with aura and without aura share the same clinical features with respect to the headache, and differ nosologically in the presence or absence of aura. The mechanisms of aura generation are now becoming clearer, based on imaging studies, and a common migraine pathophysiology for all subtypes of migraine headaches now seems reasonable, as it would seem implausible that all of these neurological events have different pathogenic mechanisms. ⋯ So what is the mechanism of migraine aura? Do migraine without aura patients have clinically silent aura? Migraine is after all defined as a clinical disorder and is the prototypic primary headache and thus its uniform pathogenesis must underlie all that we know about migraine clinically. This presentation will take the resolve that the migraine with and without aura share the same pathogenic mechanisms.