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A small number of syndromes that initially were correlated, more or less convincingly, with relevant lacunes observed at subsequent autopsy have come to be regarded as the classical lacunar syndromes (LACS), pure motor stroke (PMS), pure sensory stroke (PSS), homolateral ataxia and crural paresis (HACP), dysarthria-clumsy hand syndrome (DCHS), ataxic hemiparesis (AH), and sensorimotor stroke (SMS). The original cases of HACP were described as having weakness of the lower limb, particularly the ankle and toes, a Babinski sign, and striking dysmetria of the arm and leg on the same side. The classical LACS are clinical paradigms that should be fine-tuned by clinicians. They have been shown to be simple and reasonably valid markers for a numerically significant and pathophysiologically distinct subgroup of patients with cerebral infarction. Clinical and research utility of the classical LACS will have to be kept under review in the era of hyperacute stroke assessment and treatment.
The analysis of many different studies on the characteristics of headaches provides data to help predict the type of cerebrovascular disease according to headache patterns. Lack of headache at onset, sentinel headache, or associated vomiting is predictive of ischemic stroke. A history of throbbing headache is predictive of developing headache during a stroke. A headache preceding the cerebrovascular event (sentinel headache) has been a common occurrence in most studies, reported in up to 60% of patients. The coexistence of headache and stroke encompasses a large spectrum of possibilities, including stroke caused by migraine headache, migraine developing after a stroke, and non-migraine headache occurring in relation to stroke. A higher incidence of patent foramen ovale (PFO) in migraine with aura patients suggests that cardiac microemboli affecting the vertebrobasilar circulation may participate in the migrainous mechanisms of these patients.
The stroke–migraine interaction is one of the most fascinating and intriguing among neurological diseases. It appears obvious; however, it remains unravelled.
The coexistence of headache and stroke encompasses a large spectrum of possibilities including stroke caused by migraine headache, migraine developing after a stroke and non-migraine headache occurring in relation to stroke.
Headache occurs in approximately 200000 of the 550000 patients who have a stroke annually in the US (Vestergaard et al., 1993). Although not frequent, the bidirectional association between migraine and stroke is well known and important to recognize for diagnostic, treatment and prognostic reasons. Despite recent and significant advances in understanding of the pathophysiology linking both processes, the exact mechanisms relating migraine and stroke have not been fully elucidated.
When referring to migraine, we should think of a complex syndrome with many characteristics among which headache is the most prominent and is almost invariably – but not always – present. Migraine and stroke can result in focal sequelae and both share headache as a frequent symptom.
All the potential scenarios in the headache–stroke relationship include: (i) patients with history of migraine who at one point in their lives develop a stroke (temporally unrelated to migraine); (ii) patients with migraine who develop brain infarction during a typical migraine attack; (iii) patients who develop migraine immediately after a stroke; (iv) patients who develop migraine some time after having a stroke; (v) patients with migraine as a manifestation of vascular disease (thrombosis, vascular malformation) without the occurrence of a stroke; (vi) patients in whom migraine disappears after stroke occurrence; (vii) patients with non-migrainous headache only present at the time of a stroke; (viii) patients with non-migrainous headache following a stroke.
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