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Medication Review

Nige

Anti epileptic (to be tidied up)
Conventional and newer AEDs have showed a therapeutic efﬁcacy in CPSP treatment, even if conclusive evidences have not been published. These drugs reduce abnormal neuronal hyperexcitability through modulation of voltage-gated ion channels.
Carbamazepine (CBZ) 800 mg/day did not produce a signiﬁcant pain relief compared to placebo in 15 patients with CPSP. CBZ may be effective in paroxysmal shooting pain related to CNS but side effects (i.e. dizziness and drowsiness) have been described in 25–50% of patients, especially in the elderly [49,50]. Titration dose should be gradual, beginning with 100 mg/day and increasing
to efficacy or side effects.
Oxcarbazepine, a ketoanalogue of CBZ, may be an alternative in patients intolerant to CBZ or with significant drug interactions, but published controlled trails are lacking.
In a class I, double-blind, placebo-controlled, crossover study, 30 CPSP patients were randomized to receive lamotrigine (started at 50 mg/day and titrated up to 200 mg/day) or placebo. In 27
CPSP patients (90%) lamotrigine (200 mg/day) signiﬁcantly reduced average pain score (lamotrigine score 5; placebo score 7; p < 0.01).
Moreover, lamotrigine treatment significantly improved global pain score, duration of spontaneous pain, allodynia and dysesthesia. Adverse drug reactions were similar in both groups (57% in
lamotrigine group, 60% in control group) [51]. Therefore, lamotrigine seems to be moderately effective and well tolerated in CPSP
treatment.
Several open label studies have suggested gabapentin effectiveness in post stroke pain relief [52]. Serpell described clinical efficacy of gabapentin titrated to 2400 mg/day over 8 weeks in
9 patients with CPSP [53]. However, patients previously unresponsive to gabapentin were not included in this study and it is not clear
if all the patients had neuropathic pain.
Gabapentin (1200–3600 mg/day) may be effective in several pain components including pain paroxysms, and brush/cold induced allodynia related to both peripheral and central lesions. Several side effects may occur during titration and include
dizziness, drowsiness, and weight gain on long-term use. Therefore, in CPSP patients gabapentin treatment could not be satisfactory.
Phenytoin, zonisamide, and topiramate have been tried in a small number of patients with CPSP. Effective relief of severe, persistent pain with phenytoin (300 mg/day) has been reported in two cases of small lacunar thalamic infarction [55].
A open-label study performed in eight patients with thalamic pain showed that phenytoin was able to improve pain symptoms in 5 patients. However, in these patients phenytoin discontinuation got pain worsening [56].
Zonisamide (200 mg daily) was found to be effective in two patients with CPSP after right thalamic infarction, with no side effects [57]. Topiramate (50 mg weekly up to 200 mg
3 times daily) has been studied in three patients with CPSP refractory to carbamazepine, amitriptyline, lamotrigine, gabapentin, and mexiletine, but no patient showed CPSP relief. Side effects included
urinary sludge and lethargy [58]. There is no conclusive evidence for phenytoin, zonisamide, and topiramate effectiveness in CPSP.
Effectiveness of pregabalin (150–600 mg/day) in CPSPs was evaluated in a 13-week, randomized, double-blind, multi-centre, placebo-controlled, parallel group study, in 219 patients. Primary effectiveness endpoint was the main pain score on Daily Pain Rating Scale over the last 7 days on study drug up to 12 weeks. Secondary endpoints included other pain parameters and patient-reported sleep and health-related quality-of-life measures.
Pregabalin signiﬁcantly improved (p < 0.05) only secondary end points, compared to placebo (i.e. MOS-sleep, HADS-A anxiety, and clinician global impression of change). Adverse events were more
frequent with pregabalin than with placebo and induced treatment discontinuation was 8.2% (9 patients) in pregabalin group compared to 3.7% (4 patients) of the placebo-group. Although pain relief was not significantly different between pregabalin and placebo, its effectiveness on sleep, anxiety, and CGIC suggests that pregabalin may have a role in the management of cpsp.

Anti depressant with pain relieving properties
Amitriptyline / Nortriptyline
Nortriptyline was the forerunner of Amitriptyline.

Duloxetine

Simon

Nige In 27
CPSP patients (90%) lamotrigine (200 mg/day)

I can see why you want to include it in your medication regime…

Nige gabapentin effectiveness in post stroke pain relief

And that’s borne out by anecdotal reports…

Nige should consider polytherapy

Deffo. Indicates that a low level of specialisation by GPs would potentially yield positive results

Nige have recently emerged

Oh I thought that been around for quite a while

The way I read this and a lot of other posts that you create is that the clues are there. With detailed and exhaustive application of literature reviews - best done using AI and deep learning - new polytherapeutic approaches will be easy to postulate and have a probability of being useful without side effects that outweigh the relief

If we had a big group of folk - have you looked at patientslikeme.com ?

Caio
Simon

Nige

CPSP is a common, but underestimated, consequence of stroke. Estimated incidence between 8% and 35% is misleading, considering the enormous burden of stroke in the population. When clinicians prescribe AEDs for CPSP treatment, they should consider polytherapy and comorbidity (e.g. physiologic changes and cognitive impairment). The low number of effective AEDs in CPSP treatment suggests that a lot of mechanisms may contribute to its development. Literature data show the efficacy of lamotrigine, that may be due to its effects on noradrenergic/serotoninergic system, so it could be used as adjunctive therapy. In contrast, a recent Cochrane review of 11 publications, with only one on CPSP, did not show a lamotrigine effectiveness in the management of chronic neuropathic pain.
GABAergic drugs, such as gabapentin or pregabalin, have recently emerged as a potentially useful therapy for chronic neuropathic pain, but no conclusive data exist on central neuropathic pain. However, research supporting the effectiveness of AEDs in CPSP is still inadequate and conclusive evidences have not been published. So, more prospective clinical trials are needed to confirm the effectiveness of both conventional and newer AEDs in CPSP and to better estimate the proportion of responders in larger groups of patients. In the future, a better understanding of the effects of AEDs on CPSP should be provided by an increased knowledge of CPSP pathophysiology.

Nige

https://www.sciencedirect.com/science/article/pii/S1526590024006229

Nige

There is no hiding away from how horrendous a stroke outcome of cpsp can be. It makes the failure to adequately research and support all the more disappointing.
“Alongside complicated sensory signs, CPSP patients are also at a higher risk of developing physical and psychological comorbidities than stroke patients without CPSP. These include headaches, shoulder pain, depression, insomnia, drug dependency, and suicide. Therefore, when deciding on a treatment strategy, it is important to consider how different treatment options affect a patient’s quality of life and any comorbidities that they may have.”

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