A 25-year-old Indian woman presented to the emergency department with sudden onset of moderately severe holocranial headache. She was nauseated, but had no vomiting, neck stiffness or photophobia. She had been previously well and took the combined oral contraceptive pill. There was no family history of thrombosis. On examination, she was apyrexial with a Glasgow coma scale score of 15. There were no focal neurological signs. Routine blood tests were normal and her MRI scan of brain was initially reported as normal (figure 1). Her headache persisted and 2 days later she had a generalised tonic-clonic seizure. Repeat MRI scan of brain showed haemorrhage in the right temporal lobe (figure 2). Due to further convulsive …

ICU acquired hypernatremia (IAH) is associated with increased morbidity and mortality, however treatment remains controversial. This study aims to determine the effect of enteral free water suppletion in patients with IAH.Retrospective single center study in a tertiary ICU. Inclusion criteria: patients with IAH and treatment with enteral free water. Exclusion criteria: patients with renal replacement therapy, diabetic ketoacidosis or hyperosmolar hyperglycaemic state. Primary outcome: change in plasma sodium (in mmol/l) after 5 days treatment. Responders were defined as patients with a decrease in sodium level of 5 mmol/l or more.In total 382 consecutive patients were included. The median sodium level at the start of water therapy was 149 mmol/l (IQR 147–150). The median volume of enteral water was 4423 ml (IQR 3349–5379 ml) after 5 days and mean sodium decrease was 1.87 mmol/l (SD 4.84). There was no significant correlation between the volume of enteral water and sodium decrease (r2 = 0.01).Treatment with enteral free water did not result in a clinically relevant decrease in serum sodium level in patients with IAH. In addition, the volume of enteral free water and the use of diuretics was unrelated with sodium change over 5 days.

Normal pressure hydrocephalus is characterised by the triad of gait disturbance, dementia and urinary incontinence. Although our understanding of the condition has considerably improved since it was initially described over 50 years ago, its pathophysiology is still a matter of debate. We provide an overview of the current concepts in pathophysiology and discuss the clinical features, diagnosis and treatment of this cause of dementia.

Context: Migraine and cluster headache are undoubtedly painful conditions. The respective pathogenesis of these two conditions is incompletely understood. In both cases, the treatments used have largely been empirical and have relied to a much lesser extent on our understanding of the mechanisms causing pain. We hereby review the pain mechanisms in migraine and cluster headache, two of the commonest primary headache disorders. Evidence Acquisition: A review of the English literature was conducted by searching PubMed for studies on pain mechanism in migraine and cluster headache. We entered [migraine] and [pain mechanism] in Pubmed and 488 articles were obtained. Articles were then included according to their relevance to the topic. Similarly, [cluster headache] and [pain mechanism] revealed 79 search results. Results: There is evidence that the trigeminovascular system and neurogenic inflammation play important roles, together with certain areas of the brain, leading to these conditions being termed 'neurovascular headaches'. Functional imaging findings suggest a possible role of the dorsolateral pons in generating migraine attacks while the role of the hypothalamus in cluster headache is more firmly established. Conclusions: Migraine and cluster headache have complex pathophysiologies. The exact mechanism causing pain in both conditions is incompletely understood and more research needs to be undertaken in this area.

Thunderclap headache refers to a severe headache of abrupt onset. It is a neurological emergency with potentially catastrophic consequences and should therefore be recognized and investigated promptly. Several conditions may cause thunderclap headache. Subarachnoid haemorrhage remains the most common condition that needs to be ruled out in the first instance. When no cause is identified, the term primary thunderclap headache is used but this is a diagnosis of exclusion and should only be used after other conditions have been systematically ruled out with clinical evaluation and different imaging modalities. This review will discuss the clinically serious conditions to present as thunderclap headache that should be carefully considered.

Chronic migraine (CM) is a severe disabling condition with a few available evidence-based management options. OnabotulinumtoxinA (onaBoNTA) is approved for use in a number of disorders. Its benefits and potential use in migraine were observed incidentally while treating patients cosmetically for wrinkles. The mechanism of action of onaBoNTA in CM is not fully understood, but there is evidence that this involves axonal transport via sensory fibers. The Phase III REsearch Evaluating Migraine Prophylaxis Therapy trials have established the efficacy as well as the long-term safety and tolerability of onaBoNTA in CM. This review will discuss the evidence behind its use in this setting.

Cluster headache (CH), one of the most painful syndromes known to man, is managed with acute and preventive medications.The brief duration and severity of the attacks command the use of rapid-acting pain relievers.Inhalation of oxygen and subcutaneous sumatriptan are the two most effective acute therapeutic options for sufferers of CH.Several preventive medications are available, the most effective of which is verapamil.However, most of these agents are not backed by strong clinical evidence.In some patients, these options can be ineffective, especially in those who develop chronic CH.Surgical procedures for the chronic refractory form of the disorder should then be contemplated, the most promising of which is hypothalamic deep brain stimulation.We hereby review the pathogenesis of CH and the evidence behind the treatment options for this debilitating condition.

Migraine, a significantly disabling condition, is treated with acute and preventive medications. However, some individuals are refractory to standard treatments. Although there is a host of alternative management options available, these are not always backed by strong evidence. In fact, most of the drugs used in migraine were initially designed for other purposes. Whilst effective, the benefits from these medications are modest, reflecting the need for newer and migraine-specific therapeutic agents. In recent years, we have witnessed the emergence of novel treatments, of which noninvasive neuromodulation appears to be the most attractive given its ease of use and excellent tolerability profile. This paper reviews the evidence behind the available treatments for migraine.

The most poisonous substance known to man, botulinum toxin has successfully established itself as a therapeutic agent over the years. Initially used to treat strabismus, botulinum toxin is now an accepted treatment in a wide spectrum of disorders and has over a 100 potential medical applications. The somewhat loosely-applied term 'wonder drug' could not be better employed to describe the remedial potential of this agent. With time, and through further studies, it is likely that the number of conditions treated with botulinum toxin will keep expanding. This review will focus on the mechanisms of action of botulinum toxin and the evidence behind its use in a variety of conditions.