Parietal pseudothalamic pain syndrome. Clinical features and anatomic correlates.

We studied six patients who developed spontaneous hemibody pain following lesions of the parietal lobe. The pain was characterized as burning or icelike, and was associated with impairment of pin and temperature appreciation. Computed tomographic scanning showed that the common area of involvement in all cases was the white matter deep to both the caudal insula and the opercular region of the posterior parietal cortex. We suggest that disruption of the interconnections between these cerebral cortical areas (including the second somatosensory representation, SII) and the thalamus, particularly the intralaminar and ventroposterior nuclei, may be responsible for producing a thalamocortical disconnection syndrome with spontaneous pain as its clinical manifestation.     

Central post-stroke pain in Wallenberg syndrome]

We analyzed clinical characteristics of central post-stroke pain (CPSP), constant and burning pain, in 32 patients with Wallenberg syndrome due to infarction. CPSP developed in 44% (14/32) of the patients; 8 in acute stage (within 4 days after the stroke) and 8 in chronic stage(10-120 days after the stroke). Apart from one exceptional case, CPSP was present in the hypalgesic side of face and extremities. In 9 cases of typical type (Currier's distribution of sensory disturbance), CPSP occurred in the ipsilateral face to the lesion during acute stage. Among them, 2 cases developed severe lancinating pain in chronic stage. In 5 cases of ventral type, it occurred in the contralateral extremities during chronic stage. Spino- and trigemino-thalamic tract are injured but medullary reticular formation is intact in Wallenberg syndrome. It is, therefore, considered that CPSP in Wallenberg syndrome is caused by denervation sensitivity of "paleo-reticulothalamic" tract within the reticular formation.     

Sensorimotor retuning [corrected] in complex regional pain syndrome parallels pain reduction

Patients with complex regional pain syndrome (CRPS) and intractable pain showed a shrinkage of cortical maps on primary (SI) and secondary somatosensory cortex (SII) contralateral to the affected limb. This was paralleled by an impairment of the two-point discrimination thresholds. Behavioral treatment over 1 to 6 months consisting of graded sensorimotor retuning led to a persistent decrease in pain intensity, which was accompanied by a restoration of the impaired tactile discrimination and regaining of cortical map size in contralateral SI and SII. This suggests that the reversal of tactile impairment and cortical reorganization in CRPS is associated with a decrease in pain.     

Asperger's syndrome and cortical neuropathology

Asperger's disorder or syndrome is characterized by impaired social interaction, normal intelligence, and adequate language skills in the areas of grammar and vocabulary. The symptoms are pervasive in nature and usually manifested in childhood. Despite the gravity and chronicity of the condition, the medical literature remains sparse and offers no information about possible neuropathologic underpinnings. The present study is a case report on two patients with Asperger's syndrome. Neuropathologic examination revealed no degenerative changes or gliosis. A more detailed assessment with computerized image analysis indicated abnormalities in the minicolumnar organization of the three areas examined (9, 21, 22) (P = .032). Specifically, minicolumns were smaller, and their component cells were more dispersed than normal. A similar neuropathology has recently been reported for autism and disputes the uniqueness of these findings. The minicolumnar changes provide a possible link to receptive field abnormalities and a useful clinicopathologic correlate to Asperger's syndrome.     

Complex regional pain syndrome type I induced by phenobarbital]

Complex regional pain syndrome type I (CRPS-I) requires the presence of regional pain and sensory changes associated with findings such as abnormal skin color, temperature change, sudomotor activity, or edema, following a noxious event. Complex regional pain syndrome type I induced by phenobarbital (PB) is not well known, although several reports have strengthened the association between PB and CRPS-I. I reviewed the charts of 99 patients treated with PB to assess the incidence, clinical characteristics, investigations, dosage and plasma concentration of PB, and risk factors in the development of CRPS-I. Six patients developed CRPS-I. Pain was severe and allodynia, swelling, discoloration, sweating were present in all patients. This syndrome manifested bilaterally in some patients. Affected patients included 5 men and 1 woman between the ages of 52 and 78 (average 64.2 years). A radiograph showed demineralization in one patient. Thermography showed temperature differences between affected and unaffected limbs, although in a few patients the differences were little because of bilateral affected limbs. 99Technetium methlyene diphosphonate bone scan showed increased periarticular changes in most of the patients. The patients developed CRPS-I at 9.7 weeks (average) after PB was begun. The average time was 7.5 months between CPRS-I and PB reduction. Neither sympathetic ganglion blockade nor physical therapy was effective. Treatment of CRPS-I consists of PB reduction and prednisone and/or Neurotropin. In all patients clinical symptoms and signs such as pain and edema, and range of motion of their shoulders were improved after PB discontinuation. One patient was followed longitudinally, documenting improvement following discontinuation, reexacerbation with PB rechallenge, and remission once more when PB were discontinued. The higher incidence should depend on the coexistence of separate risk factors such as age and PB dosage. Recognition of CRPS-I induced PB, early diagnosis, and withdrawal of PB are important for symptomatic relief and improvement of QOL.     

TMS motor cortical brain mapping in patients with complex regional pain syndrome type I.

OBJECTIVE: The motor cortical representation in patients with complex regional pain syndrome type I (CRPS I) was determined under the assumption that the motor cortex undergoes representational adaptations in the course of CRPS. METHODS: A total of 14 patients with CRPS I and a group of healthy subjects without any known neurological symptoms participated in the study. The motor cortical representation, i.e. the size of representation (cm2), motor-evoked potentials (MEP), the calculated volume (cm2 mV), and the center of gravity (CoG) were measured by transcranial magnetic stimulation. Recordings were made of the long extensor muscles of the forearm of the affected and unaffected hand. RESULTS: Analyses of the results revealed a significant asymmetry between the two hemispheres: the motor cortical representation corresponding to the unaffected hand was significantly larger. While the CoG data did not differ statistically between the two hemispheres, the CoG coordinates corresponding to the affected hand indicated a larger variability. CONCLUSIONS: The presence of pain and other CRPS symptoms may induce lasting changes in motor cortical plasticity, as it also does in the sensory cortex. SIGNIFICANCE: This could be of importance in rehabilitative strategies for the sensory motor system in CRPS I patients.     

The cortical rhythms of chronic back pain

Chronic pain is maladaptive and influences brain function and behavior by altering the flow and integration of information across brain regions. Here we use a power spectral analysis to investigate impact of presence of chronic pain on brain oscillatory activity in humans. We examine changes in BOLD fluctuations, across different frequencies, in chronic back pain (CBP) patients (n = 15) as compared to healthy controls (n = 15) during resting-state fMRI. While healthy subjects exhibited a specific, frequency band-dependent, large-scale neural organization, patients showed increased high-frequency BOLD oscillations (0.12-0.20 Hz) circumscribed mainly to medial prefrontal cortex (mPFC) and parts of the default mode network. In the patients a correlation analysis related the mPFC aberrant BOLD high-frequency dynamics to altered functional connectivity to pain signaling/modulating brain regions, thus linking BOLD frequency changes to function. We also found that increased frequency fluctuations within the mPFC were temporally synchronous with spontaneous pain changes in patients during a pain-rating task. These observations provide novel insights about the nature of CBP, identifying how it disturbs the resting brain, and link high-frequency BOLD oscillations to perception.     

Chronic lumbar pain syndrome as symptomatic final stage of psychogenic conflict]

The author gives an illustrative survey of the psychosomatic aspects of chronic low back pain syndromes. On the basis of epidemiological data the social relevance of such syndromes is pointed out. Subsequent to a general clinical introduction concerning the pathogenesis and psychosomatic dynamic of symptoms in lumbar vertebral pain syndromes the author describes, by means of case reports, the essential psychodynamic conflict patterns which could be of crucial importance for the development and course of symptomatology. Risks and particular problems of the therapeutic treatment of patients suffering from chronic low back pain syndromes are finally discussed.     

Thalamic pain syndrome

Central pain is a chronic pain due to various causes, with accompanying neurological symptoms and often unresponsive to medical therapy. Pain management and results in a 31 years old female patient with a diagnosis of thalamic pain syndrome, which is one of the causes of central pain is analysed in this article.     

Myofascial pain syndrome

Myofascial pain syndrome is a regional muscle pain disorder that is the most common physical diagnosis causing chronic pain. The complex symptoms, concomitant disorders, and frequent behavioral and psychosocial contributing factors make this disorder frequently overlooked and difficult to treat. Once recognized, management programs involving rehabilitating the affected muscles and controlling the contributing factors are effective if long-term compliance is maintained by the patient.     

Patients with chronic pain exhibit individually unique cortical signatures of pain encoding

Chronic pain is characterised by an ongoing and fluctuating intensity over time. Here, we investigated how the trajectory of the patients'' endogenous pain is encoded in the brain. In repeated functional MRI (fMRI) sessions, 20 patients with chronic back pain and 20 patients with chronic migraine were asked to continuously rate the intensity of their endogenous pain. Linear mixed effects models were used to disentangle cortical processes related to pain intensity and to pain intensity changes. At group level, we found that the intensity of pain in patients with chronic back pain is encoded in the anterior insular cortex, the frontal operculum, and the pons; the change of pain in chronic back pain and chronic migraine patients is mainly encoded in the anterior insular cortex. At the individual level, we identified a more complex picture where each patient exhibited their own signature of endogenous pain encoding. The diversity of the individual cortical signatures of chronic pain encoding results bridge between clinical observations and neuroimaging; they add to the understanding of chronic pain as a complex and multifaceted disease.     

A case of Guillain-Barré syndrome starting from severe upper back pain]

Examination of a 58-year-old woman who had developed severe upper back pain showed left peripheral type of facial nerve palsy, sensory disturbance of limbs and body trunk (Th7-9), cerebellar ataxia and generalized hyporeflexia. Upper back pain increased at night and was resistant to NSAIDs, antianxiety agents, opioids, and corticosteroids. Concentrations of serum CK and cerebrospinal fluid total protein were elevated. Electromyography (EMG) of perivertebral muscles (Th7-10) showed reduced recruitment and polyphasic potential. Several days later, our patient developed weakness of limbs and respiratory failure, and required mechanical ventilation. From these findings, we diagnosed her as having Guillain-Barré syndrome (GBS) and began treatment with intravenous immunoglobulin therapy. All symptoms including upper back pain improved gradually, and she had recovered almost completely by the 40th hospitalization day. Pain, especially lower back and leg pain, have attracted attention as common symptoms in GBS. However, only one GBS patient with initial severe upper back pain has been reported. Although the precise mechanism of pain in GBS remains unclear, EMG findings lead us to surmise our patient's pain originated from the nerve roots. Limb and back pain should therefore be taken into account for the diagnosis and treatment of GBS patients.     

Gap-task模式下反射性视觉诱导性眼扫动的左侧皮层控制机制

目的研究gap-task模式下反射性视觉诱导性眼扫动的左侧皮层控制机制.方法以左侧额叶脑梗死患者、左侧顶叶脑梗死患者与正常受试者为研究对象,按照gap-task模式测定左右眼扫动速度及潜伏期,并观察眼动波形,通过组间对照以探讨该模式眼扫动的皮层控制机制.结果左侧顶叶病变患者出现双向启动延迟,但以右向眼动的受累更为显著;左侧顶叶与额叶病变均会引起右向眼扫动准确性下降.结论对于gap-task模式下反射性视觉诱导性眼扫动,左侧顶叶可以启动双向眼动,并表现出支配向右侧的眼球运动优势,额叶则不参与启动过程;左侧顶叶与额叶共同参与调节向对侧的眼球运动幅度,以保证眼扫动的准确性.