scholarly journals EVALUATION OF ANTIOXIDANT POTENTIAL AND REDUCING POWER OF CALLUS INDUCED FROM LEAVES OF ASYSTASIA GANGETICA (L.) T.ANDERSON

Author(s):  
T. G. UMESH ◽  
ABHIRAMI DILKALAL

Objective: Neuropathic pain arises from demage, or pathological changes in the peripheral or central nervous system. The pain is difficult to treat as standard treatment with conventional analgesics doesn`t typically provide effective relief of pain. Methods: It was a one year study of utilization and analysis of prescriptions for PNDs (Painful neuropathic disorders). The parameters evaluated were demographic profile of the patient (age and gender), type and etiology of PNDs, drug data (name of the group of drugs with individual drugs, mono or polytherapy, number of drugs per prescription, formulation) and associated adverse drug reactions (ADR) with the prescribed drug. Results: Maximum number of patients of PNDs resides in the age group of 18 – 35 y (41.2%) & more common in females. The most common PND encountered was painful diabetic neuropathy (43.9%) followed by cervical and lumbar radiculopathy, postherpetic neuralgia. 2942 drugs were prescribed in 1020 prescriptions, out of which 96.8% were oral and 3.2% were topical formulations. Most frequently prescribed group of the drug was tricyclic antidepressants (27.3%) followed by anticonvulsants (25.3%). Polypharmacy was seen 89.7% as compared to monotherapy (10.3%). Only 132 ADRs of various types were seen. The most common organ system affected was central nervous system followed by gastrointestinal systems. The most common drugs implicated for ADRs were TCAs (24.4%), anticonvulsants (16.6%), and Pregabeline (9.8%). There were no fatal adverse events. Mild to moderate ADRs included constipation, nausea, vomiting, drowsiness, dryness of mouth. Conclusion: The choice of drug depends on etiology of neuropathic pain, drug efficacy and availability and also on ADR profile.

Author(s):  
SUBHRANSU SEKHAR JENA ◽  
MONALISA JENA ◽  
NIBEDITA PATRO ◽  
SWATI MISHRA ◽  
MAITREYEE PANDA ◽  
...  

Objective: Neuropathic pain arises from damage or pathological changes in the peripheral or central nervous system. The pain is difficult to treat as standard treatment with conventional analgesics doesn`t typically provide effective relief of pain. Methods: It was a one-year study of utilization and analysis of prescriptions for PNDs (Painful neuropathic disorders). The parameters evaluated were demographic profile of the patient (age and gender), type and etiology of PNDs, drug data (name of the group of drugs with individual drugs, mono or polytherapy, number of drugs per prescription, formulation) and associated adverse drug reactions (ADR) with the prescribed drug. Results: Maximum number of patients of PNDs resides in the age group of 18 – 35 yrs (41.2%) & more common in females. The most common PND encountered was painful diabetic neuropathy (43.9%) followed by cervical and lumbar radiculopathy, postherpetic neuralgia. 2942 drugs were prescribed in 1020 prescriptions out of which 96.8% were oral and 3.2% were topical formulations. Most frequently prescribed group of the drug was tricyclic antidepressants (27.3%) followed by anticonvulsants (25.3%). Polypharmacy was seen 89.7% as compared to monotherapy (10.3%). Only 132 ADRs of various types were seen. The most common organ system affected was the central nervous system followed by gastro intestinal systems. The most common drugs implicated for ADRs were TCAs (24.4%), anticonvulsants (16.6%), and Pregabeline (9.8%). There were no fatal adverse events. Mild to moderate ADRs included constipation, nausea, vomiting, drowsiness, dryness of mouth. Conclusions: The choice of drug depends on etiology of neuropathic pain, drug efficacy and availability and also on ADR profile.


CNS Spectrums ◽  
2005 ◽  
Vol 10 (4) ◽  
pp. 298-308 ◽  
Author(s):  
Walter Zieglgänsberger ◽  
Achim Berthele ◽  
Thomas R. Tölle

AbstractNeuropathic pain is defined as a chronic pain condition that occurs or persists after a primary lesion or dysfunction of the peripheral or central nervous system. Traumatic injury of peripheral nerves also increases the excitability of nociceptors in and around nerve trunks and involves components released from nerve terminals (neurogenic inflammation) and immunological and vascular components from cells resident within or recruited into the affected area. Action potentials generated in nociceptors and injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected for example in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics, and do not commonly involve alterations in activity-dependent gene expression. Novel compounds and new regimens for drug treatment to influence activity-dependent long-term changes in pain transducing and suppressive systems (pain matrix) are emerging.


1940 ◽  
Vol 86 (361) ◽  
pp. 276-280 ◽  
Author(s):  
Leslie Dundonald MacLeod ◽  
Max Reiss

Since Hildebrandt (1926) described the convulsant effect of cardiazol injection, several studies have been carried out on the mechanism of such convulsions. Zung and Tremonti (1931) suggested a direct action on the respiratory centre when cardiazol is used as a stimulant; Kerr and Antaki (1937) found no effect on brain glycogen or phosphocreatine in cardiazol-induced convulsions; Hashimoto (1937) found differences in distribution of calcium and potassium ions in the central nervous system after cardiazol. Goodwin and Lloyd (1938) recorded a direct effect on brain potential changes as shown on oscillographic records. Leibel and Hall (1938) found a large (75 per cent.) diminution of cerebral blood-flow at the onset of cardiazol convulsions. Weigand (1938) found no effect on liver glycogen or vitamin A content, reducing power of suprarenal cortex or blood picture. Denyssen and Watterson (1938) and Watterson and Macdonald (1939) attribute the convulsions to action on the vasomotor centre and note the action of vasodilator drugs in inhibiting convulsions. Wortis (1938) quoted by Quastel (1939) found no effect on brain respiration.


2011 ◽  
Vol 64 (9-10) ◽  
pp. 443-447
Author(s):  
Milan Cvijanovic ◽  
Svetlana Simic ◽  
Sofija Banic-Horvat ◽  
Zita Jovin ◽  
Petar Slankamenac ◽  
...  

Introduction. Neuropathic pain, or pain associated with disease or injury to the peripheral or central nervous system, is a common symptom of a heterogeneous group of conditions, including diabetic neuropathy, trigeminal neuralgia, postherpetic neuralgia and spinal cord injury. Chronic neuropathic pain should not be thought of as a symptom. It should truly be thought of as a disease with a very complicated pathophysiology. Pathophysiology. The mechanisms involved in neuropathic pain are complex and involve both peripheral and central pathophysiologic phenomenon. The underlying dysfunction may involve deafferentation within the peripheral nervous system (e.g. neuropathy), deafferentation within the central nervous system (e.g. post-thalamic stroke) or an imbalance between the two (e.g. phantom limb pain). Clinical characteristics. Neuropathic pain is non-nociceptive, in contrast to acute nociceptive pain, and it can be described as ?burning?, ?electric?, ?tingling?, and ?shooting? in nature. Treatment. Rational polypharmacy is often necessary and actually it is almost always the rule. It would be an exception if a patient was completely satisfied with his treatment. Treatment goals should include understanding that our patients may need to be titrated and managed with more than one agent and one type of treatment. There should be the balance of safety, efficacy, and tolerability. Conclusion. There are many new agents and new applications of the existing agents being currently studied which will most certainly lead to even more improved ways of managing this very complicated set of disorders.


Cornea ◽  
2017 ◽  
Vol 36 (11) ◽  
pp. 1408-1414 ◽  
Author(s):  
Yan Xiang ◽  
Wenchang Zhou ◽  
Ping Wang ◽  
Hui Yang ◽  
Feng Gao ◽  
...  

2014 ◽  
Vol 5 (7) ◽  
pp. 525-532 ◽  
Author(s):  
Hiroshi Fukasawa ◽  
Hideaki Muratake ◽  
Ai Ito ◽  
Hideyuki Suzuki ◽  
Yohei Amano ◽  
...  

2013 ◽  
Vol 59 (1) ◽  
pp. 180-189 ◽  
Author(s):  
Robert R Langley ◽  
Isaiah J Fidler

BACKGROUND It is estimated that at least 200 000 cases of brain metastases occur each year in the US, which is 10 times the number of patients diagnosed with primary brain tumors. Brain metastasis is associated with poor prognosis, neurological deterioration, diminished quality of life, and extremely short survival. Favorable interactions between tumor cells and cerebral microvascular endothelial cells encourage tumor growth in the central nervous system, while tumor cell interactions with astrocytes protect brain metastases from the cytotoxic effects of chemotherapy. CONTENT We review the pathogenesis of brain metastasis and emphasize the contributions of microvascular endothelial cells and astrocytes to disease progression and therapeutic resistance. Animal models used to study brain metastasis are also discussed. SUMMARY Brain metastasis has many unmet clinical needs. There are few clinically relevant tumor models and no targeted therapies specific for brain metastases, and the mean survival for untreated patients is 5 weeks. Improved clinical outcomes are dependent on an enhanced understanding of the metastasis-initiating population of cells and the identification of microenvironmental factors that encourage disease progression in the central nervous system.


2010 ◽  
Vol 1 (4) ◽  
pp. 229-234 ◽  
Author(s):  
Taraneh Moini Zanjani ◽  
Masoumeh Sabetkasaei ◽  
Behnaz Karimian ◽  
Farzaneh Labibi ◽  
Babak Farokhi ◽  
...  

AbstractBackgroundEvidence for a role of immune system in hyperalgesic pain states is increasing. Recent work in neuroimmunology suggests that the immune system does more than simply perform its well known functions of recognizing and removing invading pathogens and tumors. Interest in neuroinflammation and neuroimmune activation has grown rapidly in recent years with the recognition of the role of central nervous system inflammatiom and immune responses in the aetiology of pain states. Among various theories, the role of inflammatory responses of the injured nerve has recently received attention. Cytokines are heterogenous group of polypeptides that activate the immune system and mediate inflammatory responses, acting on a variety of tissue, including the peripheral and central nervous system. Interleukin-6 (IL-6) a pro-inflammatory cytokine, is potentially important in pain aetiology, have pronociceptive actions. Neuropathic pain may be due to a primary insult to the peripheral or central nervous system. Substances released during inflammation from immune cells play an important role in the development and maintenance of chronic pain. Nimesulide, a highly selective cox-2 inhibitor, effectively reduces hyperalgesia due to peripherally administration of inflammatory agents like formalin. The safety of nimesulide was reported for some conditions in which other NSAIDs are contraindicated. Here we have determined the effect of nimesulide on pain behaviour and serum IL-6 level in chronic constriction injury (CCI) model of neuropathic pain.MethodsExperiments were carried out on male Wistar rats, (weight 150–200 g, n = 8). Rats were divided into 3 different groups: 1-CCI + saline 0.9% 2Sham + saline 0.9% (control) 3CCI + drug. Nimesulide (1.25, 2.5, 5 mg/kg, i.p.) was injected 1h before surgery and continued daily to day 14 post-ligation. 42 °C water for thermal hyperalgesia, von Frey filaments for mechanical allodynia, acetone test for cool allodynia and 10 °C water for cold hyperalgesia were respectively used as pain behavioural tests. Behavioural tests were recorded before surgery and on postoperative days 1, 3, 5, 7, 10, 14 and the serum concentration of IL-6 was determined at the day 14.ResultsThe results of this study showed a decrease in hyperalgesia and allodynia following nimesulide administration.ConclusionsIt appears that nimesulide was able to reduce pain behaviour due to nerve inflammation and a parallel decrease in the serum IL-6 concentration was observed.ImplicationsThe immune system is an important mediator in the cascade of events that ultimately results in hyperalgesia. Cytokines contribute to the patheogenesis of neuropathic pain, therefore drugs that inhibit cytokine release from immune cells may reduce inflammatory pain states.


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