Spasticity is a symptom many MS patients suffer from. But what is spasticity exactly? It is not so easy to explain in a few words: Spasticity results from the disinhibition of reflex arcs due to inflammatory lesions in the motor pathways of the brain and spinal cord. This leads to increased muscle stretch reflexes, which results in an increase in muscle tone in patients – this increase in tone is usually dependent on speed, i.e., the faster I stretch a muscle, the higher the muscle tone, or the stiffer the muscles become, which then also leads to reduced strength and endurance. The increase in muscle tone can be permanent, but it can also occur intermittently as sudden spasticity. Spasticity is often painful and results in a significant impairment of quality of life. Therefore, effective symptomatic treatment of spasticity is of great importance.There is no question that physiotherapy is an essential part of the treatment of a spastic movement disorder – it is the basis on which all further treatment strategies must build – including the drug therapy of spasticity, which I would like to discuss in more detail below. For many years, the drugs Baclofen (e.g., Lioresal®) and Tizanidine (e.g., Sirdalud®) have been available as tablet preparations for the treatment of spasticity, and in recent years Gabapentin (Neurontin®) has also been used for the treatment of spasticity. Tolperison (Viveo®) was mainly used in the new federal states, but due to a restriction of indications by the authorities, it should now only be used for spasticity after a stroke. Dantrolene and Memantine also no longer play a major role in the drug treatment of spasticity.
However, the use of cannabis preparations (see also Blog on Cannabinoids) for the treatment of spasticity in MS is becoming increasingly important. The classical antispasmodics are – despite their (supposed) side effects not having a good reputation among many patients – still an important component in the treatment of spasticity and it is sometimes disappointing that this component is not consistently used. Baclofen stimulates the GABAergic system of the spinal cord, thereby inhibiting spasticity. The substance has a wide therapeutic range and can be used in a dosage between 5 and 120 mg/day. However, the side effects of fatigue and muscle weakness are usually the limiting factors for dosing the substance higher. Nevertheless, within the therapeutic range, it is perfectly safe to “experiment” with Baclofen. In the worst case, it can lead to increased fatigue, which will pass after a short time if the dose is reduced. Because of the side effects, it is worth starting with a low dose of Baclofen (e.g., 3 x 2.5 mg) and then slowly increasing it as tolerated. The substance does not necessarily have to be taken 3 times a day, but should be used as needed to reduce spasticity situationally. The distribution throughout the day can also depend on when suffering from spasticity occurs. For some patients, this is more likely in the evening and at night, while others need a stronger effect during the day.
Accordingly, it is important that the MS patient himself – ideally in collaboration with his physiotherapist – finds out when and how he/she benefits most from an antispastic. Fixed doctor’s prescriptions without knowledge of the exact life circumstances are rather counterproductive. For Tizanidine, which attacks the alpha-adrenergic system and thus leads to muscle relaxation, the same considerations apply as for Baclofen. Sirdalud can be given in a dosage of 2 – 24 mg/day. Classic side effects, besides fatigue and muscle weakness, are also dry mouth and gastrointestinal complaints. Since Sirdalud has a different mechanism of action, it can be useful to combine Baclofen and Sirdalud. This allows the dosages of both medications to be kept lower and thus avoid side effects of the individual substances. If Baclofen and Tizanidine are poorly tolerated, Gabapentin represents an interesting therapy alternative. Gabapentin is often better tolerated, although dizziness, fatigue, and muscle weakness must also be mentioned as side effects for this active ingredient. Nevertheless, Gabapentin is also an interesting substance due to its analgesic effect, but it should be sufficiently high-dosed to achieve a corresponding effect – this is usually the case at 2400 – 3600 mg. In practice, I often observe that the substance is used at too low a dose. Especially MS patients with moderate spasticity can benefit surprisingly well from the therapies mentioned.
In cases of severe spastic paralysis, drug therapies for spasticity alone often do not suffice. In severe focal spasticity, Botulinum toxin is an important active ingredient, in severe paraspasticity of the lower extremities, the intrathecal (= administration of the substance through a needle into the spinal canal) administration of Volon A or intrathecal Lioresal administration (via a pump) play an important role. In conclusion, I would like to encourage you to approach spasticity consistently in therapy. The basis is intensive physiotherapy (the more frequent the better) – this should be supplemented by regular physical training and finally, the possibilities of drug antispastic therapy should also be used – preferably in close cooperation with your physiotherapist. I would like to encourage you to work/experiment with these medications and find out the right dose and daily distribution for you. Drug antispasmodics are certainly not miracle drugs, but they do have interesting potential for many patients.