PubMed Health⌕ Search

Biomedical subjects

Harinder Jaseja

Publications and source records attributed to Harinder Jaseja.

14 recordsLinked to original sources
PubMed2006

Treatment of interictal epileptiform discharges in cerebral palsy patients without clinical epilepsy: hope for a better outcome in prognosis.

Cerebral palsy (CP) is a motor disorder due to cerebral damage. It is commonly associated with neuro-psychological retardation and also with epilepsy; hence, its management warrants a multi-dimensional approach. In a significant number of CP patients, interictal epileptiform discharges (IEDs) are obtained in their EEG even in absence of clinical epilepsy. Epileptiform discharge-firing cortical neurons are found to be associated with elevated intracellular Ca(2+) levels and exhibition of abnormal response on exposure to excitotoxic glutamate; both these features have been found to lead to subsequent death of these neurons. This further damage is likely to aggravate the already existing cortical damage in CP patients thereby worsening their prognosis. IEDs are also known to be associated with other neuro-psychological disorders like cognitive impairment and behavioral problems even in absence of clinical epilepsy. Thus, the IEDs cannot be viewed as benign events and their occurrence even in absence of clinical epilepsy cannot be ignored. A few trials aimed at treating IEDs in autistic patients without epilepsy and in children with behavior problems have yielded favorable results. Based on these studies, the author proposes inclusion of EEG investigation in the management protocol of CP patients and treatment of IEDs (when detected even in absence of clinical epilepsy) for a better outcome in their prognosis.

Calcium Channels↗
PubMed2006

A plausible explanation for superiority of adreno-cortico-trophic hormone (ACTH) over oral corticosteroids in management of infantile spasms (West syndrome).

West syndrome (WS), an age dependent epileptic encephalopathy is identified as a triad of infantile spasms (IS), psychomotor retardation and a specific EEG pattern known as hypsarrhythmia. The exact pathophysiology still remains unclear, although a majority of cases reveal history of exposure to stress, mainly hypoxic-ischemia. The management remains empirical with a poor prognosis. Adrenocorticotrophic hormone (ACTH) and oral steroids continue to remain gold standard treatment. Vigabatrin (VGB), a newer anti-epileptic drug has emerged as an effective alternative but recent observation of a serious visual defect (constriction of peripheral field of vision that is likely to exaggerate the disability status of the WS patient) associated with its administration is gradually limiting its therapeutic usage and popularity. A number of studies have shown superiority of ACTH over oral steroids in the management of West syndrome, but the explanation for this long-standing observation is missing; however, this clinical observation has led to a wide acceptance of the implication of corticotropin releasing hormone (CRH) in causing spasms and at the same time also explaining the relief in spasms obtained by the inhibition of CRH secretion by ACTH and oral steroids. This hypothesis-article compares the negative feedback influences of ACTH and oral steroids on CRH secretion and shows that ACTH exerts a dual significantly stronger inhibitory influence on CRH secretion that far exceeds the inhibition exerted by oral steroids. Thus, this difference in feedback mechanism may be the major factor responsible for the superior therapeutic efficacy of ACTH over oral steroids in the management of West syndrome.

Administration, Oral↗
PubMed2006

Meditation potentially capable of increasing susceptibility to epilepsy - a follow-up hypothesis.

In an earlier article entitled "Meditation may predispose to epilepsy: an insight into the alteration in brain environment induced by meditation" published in Medical Hypotheses 2005:64(3):464-7, the author has hypothesized that meditation exerts predisposing influence on epileptogenesis. The hypothesis is based on certain EEG changes and electrographic features (namely hypersynchrony and coherence of EEG activity) and increase in chemical transmitters (namely glutamate and serotonin) in the brain during the course and attainment of meditation. This paper aims to further strengthen the hypothesized predisposing influence of meditation on epilepsy by providing stronger evidences and with more elaboration. Studies on meditators have reported various adverse outcomes and one such study has indeed revealed significantly higher incidence of complex partial epileptic-like signs and experiences in a large number (n = 221) of meditators compared to non-meditators (controls n = 860), the researcher claiming "cognitive kindling" by meditation to be the underlying basis. These studies thus do highlight and underscore the strong influence of meditation in increasing susceptibility to epilepsy.

Brain↗
PubMed2005

Meditation may predispose to epilepsy: an insight into the alteration in brain environment induced by meditation.

Stress-induced diseases in modern life are on an alarming rise not only in developed countries but also in developing ones. To alleviate stress, one practice that is being commonly and increasingly adapted to is meditation. Limited studies on meditation have reported occurrence of mental calmness along with apparently favorable changes in certain autonomic functional parameters like heart rate, blood pressure, respiration and skin resistance. Recently, meditation is also being practiced and advised for alleviation of epilepsy; however, very little work is available to comprehend effect and utility of meditation on epilepsy. Neuro-imaging and in-depth studies during the course and attainment of meditational state have revealed alteration in neuro-chemistry and neuro-physiology of brain environment that could favor epileptogenesis. The rise in brain glutamate and serotonin along with development of 'hypersynchrony' of EEG activity (which occur during the course and attainment of meditational state) are well documented to form the underlying basis of epilepsy. Each of the above-mentioned factors is individually capable of inducing susceptibility and decreasing threshold to epilepsy. Based on these changes in brain, this paper raises a grave possibility and risk of meditation in developing epilepsy or increasing the severity and frequency of attacks in an already epileptic state, contrary to the popular belief of its remedial role in alleviating epilepsy.

Alpha Rhythm↗
PubMed2004

Purpose of REM sleep: endogenous anti-epileptogenesis in man -- a hypothesis.

Neuro-scientists, worldwide, are endeavoring to elucidate the purpose of sleep which still remains largely elusive. There is, however, consensus on many aspects of sleep functions; one such aspect is its relationship with seizures/epilepsy. There is unequivocal agreement on increased susceptibility to epilepsy during nonrapid eye movement (NREM, slow-wave) sleep. Large number of studies have shown increased frequency of seizures and interictal epileptiform discharges in epileptic patients during NREM sleep (esp., stages I and II) which is associated with EEG synchronization. Similarly, there is widespread acceptance of de-synchronized brain-activity states being associated with rarity/total absence of epileptic potentials, one such state being rapid eye movement (REM) sleep. Certain drugs and substances which inhibit NREM sleep have been found to possess anti-convulsant properties. Not surprisingly, drugs/chemicals which enhance/promote NREM sleep or suppress/inhibit REM sleep are associated with increased susceptibility to seizures and are contraindicated in epilepsy. The manner and pattern in which REM phase occurs in sleep are also naturally programmed to exert anti-epileptogenic influence. This hypothesis-article highlights and conceptualizes the primary function of REM-sleep as endogenous anti-epileptogenic system in the body akin to the endogenous analgesia and immune systems man is born with.

Anticonvulsants↗
PubMed2004

Vagal nerve stimulation technique: enhancing its efficacy and acceptability by augmentation with auto activation and deactivation mode of operation.

The purpose of this article is to search for an additional modus operandi to improve the functioning of currently deployed vagal nerve stimulation (VNS) technique that is being used as an adjunctive therapy for intractable epilepsy, mainly complex partial seizures (partial onset with secondary generalization). The efficacy and success of current VNS technique is variable and limited, which can be attributed (to a considerable extent) to its present modi operandi. The mechanism of anti-epileptic action of VNS that has been hypothesized in the article is found to conform to observations and results in a large number of studies including those on VNS itself. Based on this mechanism in controlling seizures, the author proposes an additional mode of operation of the VNS device, (an auto activation and deactivation mode), designed to work on a feedback mechanism, which would deliver VNS as and when the brain requires it to abort/arrest the impending focal attack and/or its generalization, thus eliminating the limitations associated with the current VNS device. This mode should enhance its acceptability, efficacy and success.

Brain↗
PubMed2003

Intractable epilepsy management: an EEG-oriented approach.

Intractable epilepsy has always posed a challenge to management; conventional, surgical and alternative techniques available so far (e.g., vagal nerve stimulation, i.e. VNS). The author has attempted to search for a novel alternative (drug-regime) approach to its management to minimise any invasive technique or surgery. The drug-regime is based primarily on EEG-background picture (namely synchronisation and de-synchronisation), which the author claims plays a crucial role in epileptogenesis and/or enhancement of epileptic recruitment. Thus an EEG (both in wake and sleep states) shall be a pre-requisite. The novel drug-regime promises to alter the cortical background-activity in a manner to render it un-favorable for epileptogenesis/enhancement of epileptic recruitment, thereby attempting to produce control over Intractable Epilepsy. The new drug-regime, by virtue of its properties to alter the EEG-background activity, thus could enhance the efficacy of conventional treatment and together, they could form a highly effective management for Intractable Epilepsy, thus minimising the intervention of invasive techniques like VNS and epilepsy brain surgery.

Anticonvulsants↗
PubMed2002

Electrical resection: new concept in management of focal epilepsy.

Focal epilepsy secondary esp to scar or injured cortical tissue forms a source of constant depolarisation site with or without emitting negative charges (current of injury) into the surrounding area. This focal site is localised by EEG, MRI and if required, by PET and/or SPECT studies. The author postulates to implant electrical source of opposite charge overlying the focal site to nullify the constant depolarisation site (electrical resection) or short-circuit the current of injury to an inert site to alleviate focal epileptic attack. Preliminary trials in the form of scalp application of positivity have markedly improved EEG picture in terms of occurrence of epileptiform activity.

Brain Injuries↗