Post-Stroke Pain Syndrome
Lesions at any level of the neuroaxis (generally affecting spinothalamocortical afferent sensory pathways) including the medulla, pons, midbrain, thalamus, subcortical white matter, and the cortex may produce central pain. However, the thalamus and the brainstem are common sites for central post-stroke pain.
Thalamic post-stroke pain syndrome (Dejerine-Roussy syndrome) was first described in 1903. Eight to sixteen percent of thalamic stroke may lead to chronic pain. The frequency of pain after a geniculothalamic artery stroke is relatively higher (13% to 59%). Pain is the cardinal symptom and is described as spontaneous, severe, paroxysmal, and burning. Patients with thalamic pain syndrome also have hyperalgesia and allodynia in the affected limbs. Right-sided lesions predominate among reported cases of the thalamic pain syndrome.
Patients reporting pain due to brainstem infarction usually have involvement of pontine or medullar. Patients with midbrain infarction seldom complain of pain. Transient eye and nose pain may be manifested as an initial symptom of pontine infarction. About 25% patients with dorsolateral medullary infarction develop ipsilateral facial pain, especially when the lesion involves the spinal trigeminal tract. Facial allodynia is also common. Some patients may experience pain in the contralateral limbs and trunk.
Treatment of central post-stroke pain remains a challenge. Tricyclic antidepressants are still a choice of treatment. Gabapentin and lamotrigine have been used to treat central post-stroke pain syndrome in open labeled studies. Selective posterior rhizotomy has been reported to decrease painful spasticity in the lower limbs of hemiplegic patients after a stroke. It has been reported that chronic motor cortex stimulation therapy provides pain relief for some post-stroke patients. Thiamylal- and ketamine-sensitive and morphine-resistant cases may have more long-lasting pain reduction after chronic motor cortex stimulation therapy. Stereotactic radiosurgery of the pituitary has been used to treat thalamic pain syndrome with some success.
Forty to sixty percent of patients may develop shoulder pain after a stroke. The mechanism of shoulder pain is not clear. However, there is a strong association between pain and an abnormal shoulder joint examination, ipsilateral sensory abnormalities and arm weakness. These patients usually have significant tenderness over the shoulder joint. It is postulated that the pain is due to inflammation in the joint, secondary to immobilization and joint contracture (frozen shoulder syndrome). The majority of shoulder pain may be resolved or improved for 6 months following a stroke with intensive physical/occupational therapy. Anti-inflammatory medications may be used. Suprascapular nerve or brachial plexus block can provide temporary pain relief to prepare for physical therapy. Proper positioning of the shoulder, range of motion activities, and avoidance of immobilization may further help prevent or alleviate shoulder pain.