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The word’ thunderclap headache’ was founded by Day and Raskin in 1986. They discovered it in a patient suffering from an unruptured cerebral aneurysm who presented with multiple episodes of an abrupt onset of a severe form of headache, later labeled as a thunderclap headache.[1] A thunderclap headache is defined as a severe form of headache that occurs abruptly, like a’ clap of thunder’ as suggested by the name, peaks within 30 seconds to 1 minute of the onset, and usually fades in next few hours. It is often defined by the sufferers as the worst headache of their life.[2] Usually, thunderclap headache is the expression of intracranial vascular disorders (secondary thunderclap headache). On the other hand, it is rarely classifiable among primary headaches. Data that thunderclap headache occurs as a primary condition, indeed, is limited. Hence, primary thunderclap headache is diagnosed when all organic reasons have been ruled out.[3] A primary headache is compatible with no apparent associating etiology on the assessment of the case nor on imaging studies. According to the third edition of the International Classification of Headache Disorders (ICHD-3), the primary headache disorders are categorized as migraine, tension-type headache (TTH), trigeminal autonomic cephalalgias (TACs), and other primary headache disorders. Thunderclap headache has been documented under the’ other primary headache disorders.’ It is described as an abrupt onset severe headache which reaches a peak within a minute, lasts for at least 5 minutes, and is not better explained by other headache diagnostic criteria listed as per ICHD-3.[4] A primary thunderclap headache can be precipitated by cough, workout, and sexual activity and hence be categorized as primary cough headache, primary exercise headache, and primary headache attributed to sexual activity.[5] A thunderclap headache is continually attributed to significant vascular intracranial disorders, especially subarachnoid hemorrhage (SAH). Therefore, it should be considered a medical emergency. As a consequence, in a patient who presents in the ED with an abrupt onset of sudden severe headache, it is almost always necessary to rule out secondary causes, including significant underlying intracranial pathology like SAH, meningitis, ischemic stroke, intracerebral hemorrhage.[6] In addition to the secondary forms, primary forms of thunderclap headache can be identified, although much rarer than the secondary ones. Moreover, some authors believe that primary thunderclap headache cases may represent missed diagnoses of an underlying cause.[7][3] This chapter is aimed at presenting an overview of the features and management of the thunderclap headache. The role of the multi-professional team for improving care and patients’ outcomes is also discussed., (Copyright © 2021, StatPearls Publishing LLC.)

The white matter (WM) constitutes the network of nerve fibers that serves to allow the exchange of information and communication between different areas of the gray matter (GM). It lies beneath the GM in the brain and superficial to GM in the spinal cord. It has evolved more than GM and occupies almost half of the brain.[1] From the comparison of several cross-sections of the spinal cord performed in different regions, it is evident that the size of the area occupied by the WM varies from region to region, depending on the extent of the central GM. In particular, the GM/WM ratio grows from the cervical region to the lumbar region as the WM is decreasing as it proceeds towards the terminal portion of the spinal cord. The WM contains neural networks formed by bundles of axons to mediate essential connectivity between different key motor and cognitive cortical regions. It comprises of myelinated and unmyelinated axons along with glial cells, including myelin-producing oligodendrocytes, microglia, astrocytes, and oligodendrocyte progenitor cells. Myelin acts as electrical insulation for axons and is responsible for rapid saltatory impulse propagation and protects the nerve fibers from injury.[2] It has a water content of about 40%. The remaining dry mass (60%) is mainly composed of proteins (15% to 30%) and lipids (70% to 85%), with phospholipids, cholesterol, galactolipids, and plasmalogens in a molar ratio of 2:2:1:1.[3] The chapter of WM lesions (WMLs) or leukoaraiosis encompasses small vessel vascular brain diseases and non-vascular conditions. Any process leading to change in chemical composition, damage, or ischemia of myelinated fibers can present as WMLs on magnetic resonance imaging (MRI) that represents the gold standard for WMLs investigation. The term WM hyperintensity (WMH) is quite a descriptive expression used on MRI. These lesions are best seen as hyperintensities on T2 weighted and FLAIR (fluid-attenuated inversion recovery) sequences of MRI. FLAIR sequences have a particular role in assessing WMLs close to the ventricular margin by nullifying the cerebrospinal fluid (CSF) signal. While the WMHs are well-described on MRI, the lesions were firstly illustrated based on brain computed tomography (CT). In 1985, Hachinski in 1985 described "leukoaraiosis" as "diminished density of white matter which is seen on brain computed tomography."[4] Concerning small vessel vascular brain processes, WMLs are commonly present in MRI of asymptomatic elderly individuals typically located in periventricular (PV-WMH) and deep subcortical regions (DS-WMH). For instance, WMLs are frequently detected in people with untreated chronic hypertension. The volume of WMLs tends to increase with age from small punctate lesions to large confluent lesions. Nevertheless, although the occurrence of WMLs was initially considered a normal, age-related finding, recent investigations proved that large areas of disease in the WM of the brain must be considered as neuroimaging markers of brain frailty. Of note, various longitudinal studies described WMLs as a predictor for future risk of stroke, cognitive decline, depression, disability, and mortality in the general population.[5][6] The clinical significance of the lesions is confirmed by the results of a meta-analysis that demonstrated three times increased risk of dementia and stroke, and a doubled risk of death in people with WMLs.[7] For instance, the ischemic microvascular disease, vascular cause of WML, may cause about 45% of dementia cases and 20% of strokes. Again, WMLs are associated with poor post-stroke outcomes and increased risk of parenchymal hematoma following mechanical thrombectomy.[8][9] Apart from WMLs secondary to small vessel disease, however, these lesions are also common features of demyelinating inflammatory disorders, leukodystrophies, and degenerative disorders. Clinical aspects, prognosis, management varies according to the distribution and spread of the WM damage. This group of lesions and diseases, therefore, includes very different clinical conditions in terms of etiology, pathogenesis, pathological features, clinical presentations, imaging, and therapy. This article is aimed at discussing the clinical features and treatment of patients with several types of WMLs. The role of the interprofessional team in evaluating and treating patients is also highlighted., (Copyright © 2021, StatPearls Publishing LLC.)