by Dr. Inna Lutsenko, ESO Social Media and PR Committee, @inna_lutsenko
Prof. Julia Ferrari from Vienna, Austria and Prof. Rebecca Redwood London, United Kingdom moderated the session.
The session started with the talk of Dr. Andrea Rossetti “Post-stroke seizures: early and late”. Dr. Rossetti brought attention to the correct semiology and the poststroke seizures. Acute symptomatic seizure starts within 7d of the insult (Begh,Epilepsia 2010) and epilepsy diagnosis will be considered if a patient experienced more than one seizure (nonprovoked = not acute symptomatic = late). Recurrence risk of poststroke seizures if they already manifested is more than 60% in the following stroke 10 years (Fisher Epilepsia 2014). And the status epilepticus would be considered if the seizures are lasting longer than 5 min (generalized convulsive), ≥ 10 min (focal) (Trinka,Elepsia 2015). Stroke is considered a leading cause of epilepsy and a status epilepticus. Pathophysiology of the early seizures is described in the imbalance between excitatory and inhibitory inputs and of the late seizures in the immunological changes in TNF1.
Important notice was that the postroke seizures are often focal and non-convulsive. EEG helps to differentiate poststroke seizures from other conditions such as the TIA, stroke progression, hyperkinetic movements, drug withdrawal, syncopes and migraine. For the diagnosis first should be used thet clinical suspicion leading the neurologist to the acute EEG, which can register epileptiform discharges in 17% (Carrera, Neurology 2006). An epileptiform activity is not considered as an independent risk factor for epilepsy (Ferreira Atuesta, Ann Neurol 2021). CEEG vs rEEG does not improve prognosis (Rossetti, JAMA Neurol 2020). Perfusion imaging should also be considered in the suspicion of the seizures in the stroke onset or in the status epilepticus following the stroke (Hauf AINR 2009, Strambo J Neurol 2018, Merl UNNP 2024).
Antiepileptic medications should not be prescribed with the intention to make so called “antiseizure prophylaxis”. As an evident treatment are considered the following pharmacological considerations: enzyme inducers, but the high risk of interactions, osteoporosis and hypercholesterolemia (Minter Ellepsia 2020) and possible risk of functional impairment (PB), hypo-Na (CBZ, OXC, ESL) should not be overlooked. Enzyme inhibitor such as valproic acid is also used but the clinicians should look at the risk of interactions, osteoporosis, weight gain and the risk of encephalopathy (Loser CNS Drugs 2023).
Post stroke spasticity management was presented by Maja Villseth (Norway). The concept of the muscle overactivity was explained starting from the lesions in the CNS exactly in the corticospinal tract and/or extrapyramidal system, leading to the imbalance between excitatory and inhibitory input from the brain and the spinal cord, which gives a supranuclear «drive» to the alpha-motor neurons in the spinal cord. This leads to the increased reflex activity in muscles and to the hyperexcitability of the stretch reflex. All pathologies affecting the extrapyramidal system can cause muscle overactivity, and the indication for treatment is independent of etiology. Spasticity is a frequent stroke complication and present in 25% of the stroke patients already on day 3, appearing first at the elbow joint. Key risk factors associated with the development of spasticity are lower Barthel Index scores, severe degree of paresis, stroke-related pain, sensory deficits (Neurology. 2013 Jan Wissel J et al).
Dr. Villseth offered to regularly use the Modified Ashworth Scale, which is the tool for the measurements of the spasticity for the monitoring of the effects.
As an early (< 12 weeks!) intervention to prevent or to already treat the poststroke spasticity the early use of the Botulinum Neurotoxin (BoNT). Early BoNT may prevent severe spasticity, complications (contractures)1,3,5,6,8 and may improve rehabilitation outcome/function, no further cost for identification of predictors of spasticity development are needed. Drug costs (1-3 vials of BoNT-A1,3,56) for early BoNT treatment of PSS seems to be less expensive (lover dose of BoNT, only 50% of dose and longer duration of effect ,3,5) as BoNT treatment in the chronic poststroke spasticity phase. Sensory deficit is the key factor in the developing of the spasticity
So when treating the poststroke spasticity physicians should consider all the parts: pain relief, hygiene, involuntary movements, prevention of contractures and deformity, passive function, active function, recovery and to combine this with GAS (Goal attainment Scale) assessment.
Post-stroke depression and the role of caregivers was presented by Orla Sheehan (Dublin, Ireland). Poststroke depression is underdiagnosed and undertreated. The risk factors include genetic factors: 5-HTTLPR, STin2 VNTR, polymorphisms of serotonin transporter gene, brain-derived neurotrophic factor, gender – in 30% of th studies it was associated with the female gender, medical history: some associations for comorbidity, previous stroke, diabetes but inconsistent and psychiatric history: history of depression or family history depression associated with PSD in a number of studies. The screening tools are CES-D, Hamilton Depression Rating Scale & PHQ-9. PHQ-9 may be most practical. Optimal timing of screening remains unknown. CES-D has the highest utility out-patient setting. In in-patient settings Geriatric Depression Scale 15, Montgomery and Asberg Depression Rating Scale (MADRS) and others. Pharmacological treatment may include nortriptyline / fluoxetine which lead to improvements in depressive symptoms, ADL impairments, cognitive function & mortality.
Cochrane Review included the 56 RCTs in 4059 patients highlighting the strong support for SSRIs to reduce dependence, disability, neurological impairment, anxiety and depression. Regretfully no effect on mortality, cognitive function or motor deficits was shown. Non-pharmacological treatments such as non-invasive brain stimulation, acupuncture, behavioral and psychosocial approaches have been incorporated in some clinical guidelines. Exercise, music, light, and art therapy remain investigational, there is some evidence for Folic acid, Vitamin B1, B6 and B12 supplements.
The topic of caregiving in post stroke patients was also well presented by Dr. Sheehan.
80% of stroke survivors return to the community. Without support for daily living many stroke survivors would end up in institutional care. Most caregivers are spouses, often in their 6th decade or older, dealing with stroke patients’ difficulties in mobility, self-care, and communication, but also their cognitive impairment, depression, and personality changes. Caregivers report physical fatigue, psychological distress, loss of social relationships, financial worries, unmet needs and lack of social support. Caregiving stress / burden can result in negative emotional, social, environmental and health related difficulties for both the stroke survivor and the caregiver.
The session finished with the intensive discussion and a vivid interest from the audience, expressing the concerns regarding the recovering of the stroke patients from spasticity and dosage and combinations of the antiseizure medications. Watch an upcoming video interview with Dr.Rossetti on my Twitter account page.
