Thalamic Pain Research Articles

A Case of Thalamic Pain Successfully Treated with Kampo Medicine

Thalamic pain, one of the central painful poststroke symptoms, is a severe pain that is often intractable. A case of thalamic pain successfully treated with Kampo medicine is presented. A 65-year-old woman complained of moderate continuous and paroxysmal severe pain in the right upper and lower limbs after she had suffered from stroke. She also complained of sensory disturbance and intermittent involuntary movement. A magnetic resonance imaging scan of the brain showed an old infarction in the left thalamus. Paroxetine was administered, but it was stopped because of nausea. Etizolam was effective in reducing the pain for only about 30 minutes. Sokeikakketsuto decoction, one of the Kampo medicines, was administered orally on the basis of Kampo diagnostic criteria. Ten (10) days later, the pain had almost disappeared, and the other symptoms had also improved. This result suggested that Sokeikakketsuto could be an option for the treatment of thalamic pain under certain conditions.

Spinal Cord Stimulation for Thalamic or Central Pain

Spinal Cord Stimulation for Thalamic or Central Pain

Clinical study on acupuncture treating thalamic pain

Objective To evaluate the clinical effect of acupuncture in managing thalamic pain syndrome.

Acupuncture as Adjuvant Therapy in Thalamic Syndrome: Case Report

Cerebrovascular diseases are responsible for a large proportion of deaths in the world. Among survivors, the majority of limiting sequelae observed is motor in origin; but when sensorial pathways or centers are affected patients can evolve with sensorial changes in the body region represented by the area of the brain affected. When the affected area is related to the thalamus the patient might develop thalamic syndrome. The objective of this report was to demonstrate the use of electroacupuncture as adjuvant in the treatment of central pain, diagnosed as thalamic syndrome difficult to control with pharmacologic therapy. This is a 46 year-old female with history of ischemic stroke in the left temporoparietal region in April 2003 that evolved to right hemiparesis and hemitaxia. One year later, the patient developed continuous, insidious pain on the right side of the body with allodynia and hyperalgia, diagnosed as thalamic syndrome. In January 2006, she was admitted to the department of pain therapy and palliative care of Santa Casa de Misericórdia de São Paulo where pharmacologic treatment was instituted with poor response; she was scheduled for neurofunctional surgery. In July 2009, electroacupuncture, in an attempt to obtain better pain control, was proposed to the patient. Electroacupuncture was done on points in the scalp. After the 11(th) session, her pain was controlled, with no use of opioids or topical amitriptyline, her well-being had increased, her motor coordination improved, she presented global pain reduction, complete in hand and face. The efficacy of electroacupuncture in pain control and well-being are in agreement with modern studies which demonstrated activation of antinociceptive pathways in the brain. Controlled prospective studies are required to reaffirm and consolidate electroacupuncture as an important technique in controlling central pain.

Poster 294: The Use of Baclofen in the Treatment of Thalamic Pain Syndrome: A Case Report

Poster 294: The Use of Baclofen in the Treatment of Thalamic Pain Syndrome: A Case Report

Thalamic pain syndrome due to cytomegalovirus vasculitis in an HIV-positive child

Dejerine-Roussy syndrome, also known as the thalamic pain syndrome is a condition in which the body becomes hypersensitive to pain as a result of damage to the thalamus, a part of the brain that affects sensation. Association of this syndrome with HIV is rare with few case reports described in adults. We report a 10 year old male child who was HIV positive and had developed this syndrome due to cytomegalovirus vasculitis.

Intracranial Neurostimulation for Pain Control: A Review

Intracranial neurostimulation for pain relief is most frequently delivered by stimulating the motor cortex, the sensory thalamus, or the periaqueductal and periventricular gray matter. The stimulation of these sites through MCS (motor cortex stimulation) and DBS (deep brain stimulation) has proven effective for treating a number of neuropathic and nociceptive pain states that are not responsive or amenable to other therapies or types of neurostimulation. Prospective randomized clinical trials to confirm the efficacy of these intracranial therapies have not been published. Intracranial neurostimulation is somewhat different than other forms of neurostimulation in that its current primary application is for the treatment of medically intractable movement disorders. However, the increasing use of intracranial neurostimulation for the treatment of chronic pain, especially for pain not responsive to other neuromodulation techniques, reflects the efficacy and relative safety of these intracranial procedures. First employed in 1954, intracranial neurostimulation represents one of the earliest uses of neurostimulation to treat chronic pain that is refractory to medical therapy. Currently, 2 kinds of intracranial neurostimulation are commonly used to control pain: motor cortex stimulation and deep brain stimulation. MCS has shown particular promise in the treatment of trigeminal neuropathic pain and central pain syndromes such as thalamic pain syndrome. DBS may be employed for a number of nociceptive and neuropathic pain states, including cluster headaches, chronic low back pain, failed back surgery syndrome, peripheral neuropathic pain, facial deafferentation pain, and pain that is secondary to brachial plexus avulsion. The unique lack of stimulation-induced perceptual experience with MCS makes MCS uniquely suited for blinded studies of its effectiveness. This article will review the scientific rationale, indications, surgical techniques, and outcomes of intracranial neuromodulation procedures for the treatment of chronic pain. Key words: Motor cortex stimulation, deep brain stimulation, pain, neurostimulation

Poststroke shoulder pain in Turkish stroke patients: relationship with clinical factors and functional outcomes

The objective of this study was to assess the possible causes of hemiplegic shoulder pain (HSP) in Turkish patients with stroke, to identify the correlation between HSP and clinical factors, and to review the effects of HSP on functional outcomes. A total of 187 consecutive patients with stroke were evaluated for the presence of HSP and for the possible causes. Each patient was evaluated by clinical, radiographic, and ultrasonographic examination. Daily living activities were assessed using the Functional Independence Measure at admission and at discharge. Patients were divided into two groups, one comprising patients with shoulder pain and the other comprising patients without shoulder pain. They were then compared with respect to clinical characteristics, radiologic findings, and Functional Independence Measure scores. Shoulder pain was present in 114 (61%) patients. Of the 114 patients with pain, 71 patients showed various grades of glenohumeral joint subluxation, 70 patients had complex regional pain syndrome-type I, 70 patients had impingement syndrome, 68 patients had spasticity, 49 patients had adhesive capsulitis, and 10 patients had thalamic pain. No correlation was found between shoulder pain and clinical factors (sex, hemiplegic side, hand dominance, etiologic cause, comorbidities). The relationship between shoulder pain and adhesive capsulitis was significant (P=0.01) and also complex regional pain syndrome-type I was statistically significant (P=0.001). The group without HSP showed significantly more improvement than the group with HSP in functional outcomes (P=0.01) and the hospitalization period was significantly shorter (P=0.03). Shoulder pain is a frequent problem in patients with stroke. It is, however, often difficult to isolate a specific cause and it causes a prolonged hospitalization period and can have a negative effect on functional outcomes.

Cortical stimulation for the treatment of thalamic pain. Report of a case

Introducción: En un intento por encontrar mejores alternativas de tratamiento para el dolor central se introdujeron numerosas técnicas de estimulación. La estimulación de la corteza sensitivo-motora es una técnica efectiva para el tratamiento del dolor central. Reporte del caso: Se describe el caso de un paciente de 52 años quien sufrió un infarto talámico hace 4 años y evolucionó con dolor en el hemicuerpo derecho a predominio braquial. La medicación tradicionalmente utilizada (barbitúricos, gabapentina y opioides) no mejoró su cuadro de dolor. Debido a que el dolor talámico era intratable con la terapia convencional, se indicó la estimulación cortical. Resultados: Obtuvimos resultados favorables en el control del dolor talámico intratable de la paciente. Pudimos comparar los resultados cuando el neuroestimulador se encontraba encendido y apagado. Se logró una mejoría según la escala visual analógica, pues disminuyó de 10 a 6 puntos después de la estimulación. Conclusiones: Tanto la adecuada indicación de la técnica quirúrgica así también como la correcta identificación del área de la corteza a estimular son los elementos primordiales para el buen resultado del tratamiento.

Delusion of Oral Parasitosis and Thalamic Pain Syndrome

Delusional parasitosis is an uncommon psychiatric condition in which patients have the immutable conviction that small, living organisms, such as worms, insects, or larvae infest their skin or other organs. The authors describe a case of an unusual association of delusional parasitosis and thalamic pain syndrome after left-posterior thalamic hemorrhage. The patient initially suffered from dysesthesia and burning pain typical of thalamic pain syndrome and subsequently developed delusional oral parasitosis ("worms" infesting her mouth). Sulpiride 100 mg/day administered in addition to amitriptyline gradually improved her delusions within 3 months. The authors speculate that this specific type of delusion can be elicited by the disruption of the somatosensory pathway and that the subsequent cortical sensory deafferentiation and reorganization arising from this disruption may contribute to the development of delusional parasitosis.

Design, construction, and validation of an MRI-compatible vibrotactile stimulator intended for clinical use

Vibrotactile stimulation has been used successfully to activate the human somatosensory pathway in functional magnetic resonance imaging (fMRI) experiments. The design and characterization of these devices are of particular interest in frequency discrimination tasks and investigations of the somatopic organization of sensory areas. However, few have investigated the utility of vibrotactile stimulation in a clinical context. We have previously demonstrated that vibrotactile stimulation can provide robust activations in areas targeted in stereotactic functional neurosurgical procedures used for tumour resection (i.e.: primary and secondary somatosensory areas) and subcortical targets for thalamic pain and movement disorders (i.e.: sensory thalamus). The main contribution of this manuscript is the presentation of the design, materials, construction, and validation of a novel vibrotactile stimulator intended for clinical use. The thalamic activations are also compared to a digital atlas in order to evaluate anatomical localization. The proposed stimulator was constructed entirely from non-ferromagnetic parts, uses compressed air to deliver stimulation using computer control, and stimulates the entirety of the hand and fingers to ensure robust somatosensory activations. In addition, this stimulator is constructed entirely from “off-the-shelf” parts and would be easily replicated due to the simplicity of design and the relatively small expense of the parts required. The device was tested by stimulating the right hand of 10 normal controls (5 females, 5 males, all right handed; age range: 25–42 years, mean: 30.9 years, standard deviation: 5.2 years) during an fMRI experiment. The results demonstrate significant single subject activations of primary and secondary somatosensory cortices and of the sensory thalamus.

Spinal Cord Stimulation and Thalamic Pain: Long-term Results of Eight Cases

Objectives. We submit a retrospective analysis of results of eight patients suffering from intractable pain of established or suspected thalamic origin. These patients were treated with spinal cord stimulation (SCS) in the cervical or dorsal cord. No patient was suffering pain from a complete hemibody or facial area. Material and Methods. Five men and three women aged 27-67 years were treated in the Pain Unit of our institution between April 1993 and January 2006. The cause of pain in five cases was stroke (plus one suspected). Multiple sclerosis was responsible for pain in two cases. An upper or lower extremity was affected in six cases. Extension to adjacent trunk was common. Exclusive trunk pain was treated in two cases. Results. The follow-up period was 36-149 months. Two patients were not battery-implanted because pain relief was insufficient during the trial phase. Two patients had a further stroke: One died and one was cured from pain. Good-to-excellent results were attained in six patients; long-term good-to-excellent results were maintained in three patients. Conclusions. Despite previous adverse reports, certain cases of thalamic pain can be effectively alleviated through SCS.

Development and characterization of a hemorrhagic rat model of central post-stroke pain

Stroke is the leading cause of disability in the industrialized world and it is estimated that up to 8% of stroke victims suffer from some form of central post-stroke pain (CPSP). Thalamic syndrome is form of central pain that typically results from stroke in the thalamus. In the present study, we describe the development and characterization of a rat model of thalamic CPSP. This model is based on a hemorrhagic stroke lesion in the ventral posterolateral nucleus of the thalamus, one of the reported causes of thalamic syndrome in humans. Behavioral analysis showed that animals displayed hyperesthesia in response to mechanical pinch stimulation, with sensitivity localized to the hind limb. This response appeared within 7 days of the intra-thalamic hemorrhage. Animals also showed increased thermal sensitivity in the contralateral hind limb. Histopathology indicated the presence of activated microglia adjacent to the core of hemorrhagic lesions in the thalamus. Neutrophils were confined to the hemorrhage core, indicating that they entered in the initial bleed. By 7 days, bands of activated microglia and astrocytes separated the hematoma from surviving neurons at the edge of the lesion. We did not observe any terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive neurons beyond the immediate hematoma at 1, 3, or 7 days after hemorrhage. Surviving neurons were located in the vicinity of activated microglia and astrocytes at the outer edge of the hematoma. Thus, thalamic hemorrhage produces a confined lesion that destroys the tissue within the initial bleed, with little or no neuron death beyond the hemorrhage core. Surviving neurons surrounded by activated glial cells likely contribute to neuropathic pain in this model. This thalamic hemorrhage model is useful for studying the neuropathology and physiology of thalamic syndrome, and developing therapeutics for central post-stroke pain.

Post-traumatic headache: facts and doubts

The International Classification of Headache Disorders does not separate the moderate from severe/very severe traumatic brain injury (TBI), since they are all defined by Glasgow coma scale (GCS) < 13. The distinction between the severe and very severe TBI (GCS < 8) should be made upon coma duration that in the latter may be longer than 15 days up to months in the case of vegetative state. Post-traumatic amnesia duration may double the coma duration itself. Therefore, the 3-month parameter proposed to define the occurrence or resolution of post-traumatic headache (PTH) appears inadequate. Following TBI, neuropathic pain, central pain, thalamic pain, combined pain are all possible and they call for proper pharmacological approaches. One more reason for having difficulties in obtaining information about headache in the early phase after regaining consciousness is the presence of concomitant medications that may affect pain perception. Post-traumatic stress disorder (PTSD) develops days or weeks after stress and tends to improve or disappear within 3 months after exposure; interestingly, this spontaneous timing resembles that of PTH. In our experience the number of TBI patients with PTH at 1-year follow-up is lower in those with longer coma duration and more severe TBI. Cognitive functioning evaluated after at least 12 months from TBI, showed mild or no impairment in these patients with severe TBI and PTH, whereas they have psychopathological changes, namely anxiety and depression. The majority of patients with PTH after severe/very severe TBI had skull fractures or dural lacerations and paroxystic EEG abnormalities. The combination of psychological changes (depression and anxiety) and organic features (skull fractures, dural lacerations, epileptic EEG abnormalities) in PTH may be inversely correlated with the severity of TBI, with prevalence of psychological disturbances in mild TBI and of organic lesions in severe TBI. On the other hand, only in severe TBI patients with good cognitive recovery the influence of the psychopathological disorders may play a role. In fact, the affective pain perception is probably related to the integrity of cognitive functions as in mild TBI and in severe TBI with good cognitive outcome.

Thalamic stroke: correlation of clinical symptoms, somatosensory evoked potentials, and CT findings.

We studied 18 patients with a single ischemic thalamic lesion, who had somatosensory disturbances and/or central pain in the opposite hemibody, by correlating their clinical symptoms, somatosensory evoked potentials (SEPs), and computed tomography (CT) findings. Patients were divided into three groups: (1) those with somatosensory deficits, central pain, and abnormal SEPs, which comprised two thirds of the patients (classic thalamic pain syndrome), (2) those with somatosensory deficits, no central pain, and abnormal SEPs (analgetic thalamic syndrome), and (3) those with almost normal sense perception, central pain, and normal SEPs (pure algetic thalamic syndrome). CT evidence of a paramedian or anterolateral thalamic lesion might be an indicator for the development of central pain, because these types of infarctions occurred only in patients with the classic thalamic syndrome or the pure algetic thalamic syndrome. The differentiation of the thalamic syndrome into three subtypes is of prognostic value, because patients with a loss of cortical SEPs and a posterolateral ischemic thalamic lesion on the CT scan probably will not exhibit central pain.

Evoked response studies of the thalamic pain syndrome.

Human and animal studies have suggested that the occurrence of thalamic pain (hyperpathia) is not simply a manifestation of a functional deficit in the major lemniscal pathway mediated through the ventral posterior (VP) thalamic nucleus. More effective relief of this pain has occurred following stereotaxic lesions of the centromedianum (CM) than after lesions restricted to VP. Median nerve stimulation has evoked abnormal contralateral somatosensory evoked responses (SER) in patients with lesions of VP. In this study the SERs evoked by contra-lateral stimulation in two patients with thalamic pain secondary to infarction were normal. These results support the hypothesis that thalamic pain can be caused by thalamic lesions sparing VP. The minor change noted in the ipsilateral SER when the abnormal hand was stimulated was consistent with a lesion involving CM or adjacent nonspecific thalamic nuclei.

Usefulness of gamma knife pituitary surgery to control thalamic pain after treatment of thalamic malignant lymphoma and report of pathology of gamma knife lesions

Here, we describe the first reported autopsy findings following gamma knife surgery for thalamic pain. A 62-year-old man presented with thalamic pain after treatment for thalamic malignant lymphoma. He was treated with narcotic drugs, but his pain was uncontrollable. Treatment using gamma knife surgery on the pituitary gland using a maximum dose of 180 Gy, led to the control of his intractable pain with lower doses of drugs. His death was pain-free and was caused by a recurrence of the tumor, six months after gamma knife surgery. An autopsy was performed and necrosis was present in the area of the pituitary gland where it borders the pituitary stalk. Half of the adenohypophysis was not necrotic, and necrosis was not found in the pituitary stalk.

Síndrome de Déjerine-Roussy de origen isquémico en un adolescente con foramen oval permeable

Déjerine-Roussy syndrome, or thalamic syndrome, is characterised by transient mild hemiparesis, hemichoreoathetosis, hemihypoesthesia, hyperalgesia, allodynia and hemiataxia with astereognosia that varies in intensity, and it appears in the presence of lesions in the posterior nuclei of the thalamus. It can be produced by strategic cerebral infarction, reported in elderly patients with vascular risk factors. Patent foramen ovale has been suggested as a risk factor for ischaemic stroke in young people, especially when associated to aneurysm of the auricular septum and above all to a procoagulating status.An 18-year-old male with a family history of Behçet's disease, who presented right-side thalamic and hippocampal cerebral infarction; following an exhaustive study, patent foramen ovale with septal aneurysm was found as the only risk factor. At that time he did not satisfy criteria for Behçet's disease, and thorough systemic screening did not reveal direct or indirect signs of venous thrombosis. Percutaneous closure of the foramen was performed.This is the first reported case of Déjerine-Roussy syndrome as a manifestation of cryptogenic cerebral infarction associated to patent foramen ovale in an adolescent. Taken as a whole, the clinical and complementary data enable us to reconstruct the pathophysiological sequence that position foramen ovale with an associated septal 'aneurysm' as the only detectable risk factor, which, when linked to the stress of the patient and the family, triggered its early closure.

Physiology and Treatment of Pain

Physiology and Treatment of Pain

(261) Use of an implantable intrathecal morphine pump in the treatment of refractory pain caused by Thalamic Syndrome

(261) Use of an implantable intrathecal morphine pump in the treatment of refractory pain caused by Thalamic Syndrome