Thalamic pain syndrome

INTRODUCTION

Thalamic pain syndrome is an unfortunate outcome following a cerebrovascular accident (CVA). After a cerebrovascular accident, the terrible symptom known as thalamic pain syndrome develops (CVA). The patient reports central, neuropathic pain that is correlated with temperature fluctuations. Patients frequently experience allodynia and hyperalgesia. Up to 8% of stroke patients will experience thalamic pain syndrome, which is a pretty significant prevalence. Despite being frequent after a stroke, diagnosis is frequently challenging. After a CVA, a patient's symptoms frequently take longer to manifest. A person who has experienced a CVA of the thalamus might not feel any discomfort at all for months or even years following their stroke. Thalamic pain syndrome was formerly known as Dejerine-Roussy syndrome, but it is now more generally referred to as central post-stroke pain.

ETIOLOGY

The most frequent cause of thalamic pain syndrome is a cerebrovascular injury. A lacunar infarct is a discrete thalamic infarction. In contrast, a larger and more severe stroke is often referred to as an infarction of the middle cerebral artery (MCA), which is a more important wounded artery. However, similar to thalamic pain syndrome, a thalamic lesion or abscess can also result in sensory impairments. Both an ischemic stroke and a hemorrhagic stroke can result in thalamic pain syndrome. Thalamic stroke sufferers report neuropathic discomfort. Any thalamic injury can result in deficiencies in the contralateral senses. Deficits in thermoregulation are caused by damage to the spinothalamic tract.

Symptoms and signs

The most typical precursor to Dejerine-Roussy syndrome is numbness on the affected side. In these situations, numbness is replaced by stinging and burning sensations that vary greatly in intensity from case to case. Hypersensitivity can also cause burning and tingling, typically in the form of allodynia or dysaesthesia. Less frequently, some individuals have excruciating, continuous pain with few or no stimulation. Pain from a stimulation that otherwise would not induce pain is known as allodynia. One sufferer, for instance, feels excruciating discomfort whenever a wind brushes his skin. Most allodynia sufferers feel discomfort with touch and pressure, but some can also be overly sensitive to temperature.

An unpleasant, abnormal feeling of touch is referred to as dysaesthesia. It frequently manifests as pain. Thalamic lesioning is the cause of this disorder. This type of neuropathic pain might include any itch, tingling, burning, or scorching sensation that is either spontaneously experienced or brought on by stimuli. Between a week and a few months following a thalamic stroke, allodynia and dysaesthesia take the place of numbness. In general, once pain has ceased developing, its form and intensity won't change over time and, if left untreated, will last the rest of one's life. As a result, many people will receive pain relief in some way and try to adapt to their new lifestyles as best they can.

Dejerine-Roussy syndrome-related pain can occasionally be accompanied by anosognosia which can lead a patient who has had a right-parietal, or right-sided stroke to deny any left-side paralysis when in fact there is, or to deny the paralyzed limb belong to them.

Mechanism

Although there are several risk factors and contributing factors for strokes, there are comparatively few for Dejerine-Roussy syndrome and thalamic lesions. Strokes typically affect one hemisphere of the brain, which includes the thalamus. It is generally accepted that the thalamus transmits sensory information to the cerebral cortex from a variety of subcortical regions. It is well known that the thalamus processes sensory data from environmental stimuli before sending it to the somatosensory cortex for interpretation. The end result of this connection is the brain's interpretation of what you can see, hear, or feel.

Tactile perception is most frequently compromised by Dejerine-Roussy syndrome. Therefore, the thalamus's injury results in a breakdown in communication between the afferent pathway and the brain's cortex, altering what or how one feels. A sensation may change in the wrong way, or it may be amplified or dulled in the wrong way. Without brain mapping and individualized counselling, it is nearly impossible to predict how a sensation would alter because the brain is thought to be malleable and each person's brain is unique. Magnetic resonance imaging (MRI) has recently been used to connect lesion size and location with affected region and ailment severity. These preliminary results show promise for a scientific method to comprehend and care for people with Dejerine-Roussy syndrome.

Epidemiology

8% of all stroke patients will experience central pain syndrome, with 5% experiencing moderate to severe pain. The risk of developing Dejerine–Roussy syndrome is higher in older stroke patients, about 11% of stroke patients over the age of 80.

Treatment

§ Antidepressants, anticonvulsants, and opioid analgesics are common treatments for concentrated and chronic pain. There is insufficient evidence to support the use of amitriptyline, opioids, anticonvulsants, transcranial magnetic stimulation, and acupuncture in the management of central post-stroke pain, according to a systematic review and meta-analysis. For situations that are resistant to other treatments, deep brain stimulation may be a possibility. Another effective therapeutic option for cases of central post-stroke pain is radiation therapy. After a CVA, cognitive-behavioral treatment helps patients avoid developing depression.

§ Desensitization to the painful tactile stimulation is the first line of treatment for central post-stroke pain. The medicine most extensively researched for treating central post-stroke pain is amitriptyline. Additionally, venlafaxine and trazodone are factors. Although results are inconsistent, SSRI antidepressants are mostly ineffective.

§ Anticonvulsants are used as a second-line therapy. For central post-stroke pain, studies on gabapentin, pregabalin, carbamazepine, phenytoin, and lamotrigine have all been conducted. In post-stroke pain syndromes, opioid analgesics, clonidine, mexiletine, and beta-blockers have all been employed. Studies have also been conducted on intrathecal baclofen and ketamine as well as lidocaine, naloxone, and propofol intravenous infusions.

§ Lamotrigine appears to be the most effective anticonvulsant for treating central post-stroke pain, according to the available data. Patients with concomitant depression and spinal cord damage respond better to amitriptyline.

§ For patients with post-stroke fatigue who have had symptoms for longer than three months, modafinil is a possibility. In addition to lowering fatigue, modafinil also enhances quality of life.In individuals with central post-stroke pain, intravenous lidocaine does provide short-term analgesia for up to 45 minutes after an infusion.

§ An additional therapy option is transcranial magnetic stimulation (TMS). Treatment with motor cortex stimulation is efficient, particularly for individuals with facial pain. Other treatments include deep brain stimulation and motor cortex stimulation. While motor cortex stimulation is successful in about one-third of individuals with central post-stroke pain, deep brain stimulation has had mixed outcomes. Compared to other types of pain, deep brain stimulation is less successful at treating central neuropathic pain.

§ Thalamotomy is a method to turn off the patient's pain's source; neurosurgery is frequently the last option. Allodynia is improved with thalamotomy and mesencephalic tractotomy. In some circumstances, the dorsal root entrance zone is also lesioned. Two years after the treatment, there is a very significant recurrence rate, nevertheless.

§ In cases where a patient is suffering from paroxysmal shooting pains, surgery is most effective. With spinal cord stimulation for central pain problems, the pain-relieving effects wear off over time.