JNS.jpgThe April issue of the Journal of the Neurological Sciences Vol 375 is now available online.


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Issue highlights

New hearts for Friedreich patients

Most individuals with Friedreich ataxia (FRDA) have an abnormal electrocardiogram and elevated serum concentrations of cardiac troponin 1. Many eventually develop cardiac hypertrophy, and heart failure is a frequent cause for their death. Histological evaluation of the heart shows enlarged cardiomyocytes encircled by fibrotic endomysium. Some of the enlarged cardiac myocytes, and also some macrophages that have accumulated in endomysium, contain iron-positive inclusions, but total cardiac iron content is not increased.


Study of SOCS gene family expression profile in MS patients: Another step forward

Multiple sclerosis (MS) is presumably an immune-mediated neuro-inflammatory and neurodegenerative of the central nervous system, which causes irreversible loss of neurons, oligodendrocytes, and myelin sheath. Despite extensive scientific research into the origin of MS, its exact cause remains elusive and our understanding of its pathophysiology remains only partial. One group of players in pathogenesis of MS is cytokines and their imbalanced interactions may promote or improve the course of MS. In the current study, the authors have attempted to examine individual cytokine signaling pathways, evaluating suppressor of cytokine signaling (SOCS), to determine the expression levels of each in blood samples of a group of 50 patients with multiple sclerosis compared to 50 healthy controls.


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Acquired pendular nystagmus

Acquired pendular nystagmus is comprised of quasi-sinusoidal oscillations of the eyes significantly affecting gaze holding and clarity of vision. The most common causes of acquired pendular nystagmus include demyelinating disorders such as multiple sclerosis and the syndrome of ocular palatal tremor. However, several other deficits, such as pharmacological intoxication, metabolic and genetic disorders, and granulomatous disorders can lead to syndromes mimicking acquired pendular nystagmus. Study of the kinematic features of acquired pendular nystagmus has suggested a putative pathophysiology of an otherwise mysterious neurological disorder. Here we review clinical features of neurological deficits that co-occur with acquired pendular nystagmus. Subsequent discussion of the pathophysiology of individual forms of pendular nystagmus speculates on mechanisms of the underlying disease while providing insights into pharmacotherapy of nystagmus.


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Vision loss in tuberculous meningitis

Vision loss is a disabling complication of tuberculous meningitis. Approximately, 15% of survivors are either completely or partially blind. All structures of the visual pathway may be affected in tuberculous meningitis. Optic nerve and optic chiasma are most frequently and dominantly affected. Thick-gelatinous exudates lying over the base of brain, are the pathological hallmark of tuberculous meningitis and are responsible for almost all of its major complications, including vision loss. Strangulation of optic nerves and optic chiasma by the exudates, compression over optic chiasma by the dilated third ventricle, raised intracranial pressure, endarteritis, shunt failure, bacterial invasion of optic nerves and drug-induced optic nerve damage are important reasons that are considered responsible for vision loss. Prompt antituberculosis treatment is the best management option available. Immunomodulatory drugs and cerebrospinal fluid diversion procedures are of limited help. Early recognition and treatment of tuberculous meningitis is the only way forward to tackle this problem.