A 51-year-old male was admitted in our institute following an episode of near-drowning. He later developed ventriculitis and cerebral ring-enhancing lesions. He died following a subarachnoid hemorrhage due to rupture of a mycotic aneurysm involving the right fetal posterior cerebral artery. Scedosporium apiospermum was isolated from the cerebrospinal fluid. Central nervous system invasion by S apiospermum may present insidiously in near-drowning patients and, therefore, requires a high index of suspicion. In cases with the characteristic cerebral ring-enhancing lesions and concomitant ventriculitis, treatment should be instituted while awaiting fungal culture. With this article we intend to alert neurologists, intensivists, and physicians to this near fatal infection, as early identification and prompt treatment with voriconazole may be life saving.

A 44-year-old male developed acute fulminant hepatic failure of unknown etiology and expired within four days. His serial electroencephalograms (EEGs) showed diffuse background slowing on day one, which evolved into “alpha coma” and later into “spindle coma” over the ensuing two days. Such EEG transition is hitherto undescribed in patients with hepatic encephalopathy and gives fresh insight into the etiopathogenesis of specific EEG patterns in diffuse encephalopathy.

Status epilepticus (SE) is a medical emergency associated with significant morbidity and mortality. SE is defined as a continuous seizure lasting more than 30 min, or two or more seizures without full recovery of consciousness between any of them. Based on recent understanding of the pathophysiology, it is now considered that any seizure that lasts more than 5 min probably needs to be treated as SE. GABAergic mechanisms play a crucial role in terminating seizures. When the seizure persists, GABA-mediated mechanisms become ineffective and several other putative mechanisms of seizure suppression have been recognized. Early treatment of SE with benzodiazepines, followed if necessary by fosphenytoin administration, is the most widely followed strategy. About a third of patients with SE may have persistent seizures refractory to the first-line medications. They require aggressive management with second-line medications such as barbiturates, propofol, or other agents. In developing countries where facilities for assisted ventilation are not readily available, it may be helpful to use nonsedating antiepileptic drugs (such as sodium valproate, levetiracetam, or topiramate) at this stage. It is important to recognize SE and institute treatment as early as possible in order to avoid a refractory state. It is equally important to attend to the general condition of the patient and to ensure that the patient is hemodynamically stable. This article reviews current knowledge regarding the management of convulsive SE in adults.

Myotonic syndromes and periodic paralyses are rare disorders of skeletal muscle characterized mainly by muscle stiffness or episodic attacks of weakness. Familial forms are caused by mutation in genes coding for skeletal muscle voltage ionic channels. Familial periodic paralysis and nondystrophic myotonias are disorders of skeletal muscle excitability caused by mutations in genes coding for voltage-gated ion channels. These diseases are characterized by episodic failure of motor activity due to muscle weakness (paralysis) or stiffness (myotonia). Clinical studies have identified two forms of periodic paralyses: hypokalemic periodic paralysis (hypoKPP) and hyperkalemic periodic paralysis (hyperKPP), based on changes in serum potassium levels during the attacks, and three distinct forms of myotonias: paramyotonia congenita (PC), potassium-aggravated myotonia (PAM), and myotonia congenita (MC). PC and PAM have been linked to missense mutations in the SCN4A gene, which encodes α subunit of the voltage-gated sodium channel, whereas MC is caused by mutations in the chloride channel gene (CLCN1). Exercise is known to trigger, aggravate, or relieve symptoms. Therefore, exercise can be used as a functional test in electromyography to improve the diagnosis of these muscle disorders. Abnormal changes in the compound muscle action potential can be disclosed using different exercise tests. Five electromyographic (EMG) patterns (I-V) that may be used in clinical practice as guides for molecular diagnosis are discussed.