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Background: Central neuropathic pain syndromes are a result of central nervous system injury, most commonly related to stroke, traumatic spinal cord injury, or multiple sclerosis. These syndromes are distinctly less common than peripheral neuropathic pain, and less is known regarding the underlying pathophysiology, appropriate pharmacotherapy, and long-term outcomes. The objective of this study was to determine the long-term clinical effectiveness of the management of central neuropathic pain relative to peripheral neuropathic pain at tertiary pain centers. Methods: Patients diagnosed with central (n=79) and peripheral (n=710) neuropathic pain were identified for analysis from a prospective observational cohort study of patients with chronic neuropathic pain recruited from seven Canadian tertiary pain centers. Data regarding patient characteristics, analgesic use, and patient-reported outcomes were collected at baseline and 12-month follow-up. The primary outcome measure was the composite of a reduction in average pain intensity and pain interference. Secondary outcome measures included assessments of function, mood, quality of life, catastrophizing, and patient satisfaction. Results: At 12-month follow-up, 13.5% (95% confidence interval [CI], 5.6-25.8) of patients with central neuropathic pain and complete data sets (n=52) achieved a ≥30% reduction in pain, whereas 38.5% (95% CI, 25.3-53.0) achieved a reduction of at least 1 point on the Pain Interference Scale. The proportion of patients with central neuropathic pain achieving both these measures, and thus the primary outcome, was 9.6% (95% CI, 3.2-21.0). Patients with peripheral neuropathic pain and complete data sets (n=463) were more likely to achieve this primary outcome at 12 months (25.3% of patients; 95% CI, 21.4-29.5) (p=0.012). Conclusion: Patients with central neuropathic pain syndromes managed in tertiary care centers were less likely to achieve a meaningful improvement in pain and function compared with patients with peripheral neuropathic pain at 12-month follow-up.
The syndrome of Wernicke's encephalopathy consists of two of four features of (1) dietary deficiency; (2) oculomotor abnormality; (3) cerebellar dysfunction; and (4) confusion or mild memory impairment. Predisposing risk factors include alcoholism, hyperemesis gravidarum and prolonged intravenous feeding.
A 35-year-old female developed refractory emesis, severe weight loss, and hypokalemia following banded gastroplasty for morbid obesity. Reversal of gastroplasty was performed four months following initial surgery. Following reversal, the patient developed confusion, ataxia, leg weakness and nystagmus.
Examination of the patient demonstrated disorientation with confusion, vertical nystagmus worse on downgaze, diffuse weakness of the lower extremities, and bilateral dysmetria. Magnetic resonance imaging of the brain demonstrated symmetrical areas of increased T2 signal present bilaterally in the medial thalamic nuclei. The patient did not demonstrate any initial improvement with intravenous thiamine but improved over two months of follow-up.
Wernicke's encephalopathy has been reported in the European literature as a complication of gastroplasty, with rare recognition of this clinical entity in the North American literature. This potential complication of gastroplasty may be preventable by nutritional intervention in subjects experiencing severe weight loss and emesis following surgery.
Background: Painful diabetic neuropathy (PDN) is a frequent complication of diabetes mellitus. Current treatment recommendations are based on short-term trials, generally of ≤3 months’ duration. Limited data are available on the long-term outcomes of this chronic disease. The objective of this study was to determine the long-term clinical effectiveness of the management of chronic PDN at tertiary pain centres. Methods: From a prospective observational cohort study of patients with chronic neuropathic non-cancer pain recruited from seven Canadian tertiary pain centres, 60 patients diagnosed with PDN were identified for analysis. Data were collected according to Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials guidelines including the Brief Pain Inventory. Results: At 12-month follow-up, 37.2% (95% confidence interval [CI], 23.0-53.3) of 43 patients with complete data achieved pain reduction of ≥30%, 51.2% (95% CI, 35.5-66.7) achieved functional improvement with a reduction of ≥1 on the Pain Interference Scale (0-10, Brief Pain Inventory) and 30.2% (95% CI, 17.2-46.1) had achieved both these measures. Symptom management included at least two medication classes in 55.3% and three medication classes in 25.5% (opioids, antidepressants, anticonvulsants). Conclusions: Almost one-third of patients being managed for PDN in a tertiary care setting achieve meaningful improvements in pain and function in the long term. Polypharmacy including analgesic antidepressants and anticonvulsants were the mainstays of effective symptom management.
Background: We set out to determine whether separable visual and representational components underlie normal subjects’ upward and distal biases in bisecting vertical and radial lines under visual guidance. Methods: Thirty-four normal subjects were asked to bisect lines oriented horizontally, vertically, and radially. Human silhouette figures were placed at either end of each line. These figures were presented upright or upside down in order to pictorially define a “top” to each line independent of the actual top of the visual field. Results: Although subjects erred toward the top of the visual field, they also demonstrated a significant bias toward the heads of the figures for lines in all spatial orientations. Conclusions: This result supports the existence of two biases: one toward the upper visual field, and another toward an internally represented “top” as suggested pictorially. These findings provide further support for the hypothesis that normal subjects’ upward and distal biases on bisection of vertical and radial lines under visual guidance have both representational and visual-based components.
To describe the clinical and laboratory findings in cases of neonatal herpes simplex virus (HSV) encephalitis.
Neonatal HSV encephalitis is a devastating infection which requires a high degree of clinical suspicion and rapid initiation of antiviral therapy.
We performed a retrospective search for all cases of HSV encephalitis within the two Saskatchewan pediatric tertiary care centers for the period of 1985-2001. Only those patients with consistent clinical presentations along with direct evidence of presence of HSV, such as positive cerebrospinal fluid (CSF) viral cultures, positive polymerase chain reaction (PCR) for HSV from CSF, or positive immunoglobulin G against HSV from neonatal blood, were selected.
Five male and four female infant patients were identified. At a mean age of presentation of 24±20 days, seizures occurred in six neonates, lethargy in six neonates, temperature changes in five neonates, and apnea in three neonates. Examination of CSF demonstrated an initial monocytosis or lymphocytosis, elevated CSF protein and depressed CSF glucose in 100% of patients. Electroencephalography (EEG) was abnormal in 100% of patients. Initial computerized tomography was abnormal in 55% of patients. Clinical follow-up over an average of two years demonstrated developmental delay in four patients and upper motor neuron findings in four patients. No patients suffered from postencephalitic epilepsy or mortality.
Neonatal HSV encephalitis most commonly presents with seizures, lethargy, and dysthermia. Cerebrospinal fluid testing and EEG have 100% sensitivity in cases with laboratory confirmation of HSV presence. Improvements in morbidity and mortality as compared to previous reports may relate to better recognition of this illness and acyclovir therapy. The lack of postinfection epilepsy in our series may also relate to better recognition and acyclovir therapy within this series of patients.
This chapter describes the forms of assessment of neuropathic pain (NP) currently used in neuropathic pain therapeutic trials including intensity scales, specific and non-specific pain measurement questionnaires, and quantitative sensory testing (QST), with emphasis on their advantages and limitations. The lack of specificity of the McGill Pain Questionnaire (MPQ) and SF-MPQ for neuropathic pain has led to the development of various NP measurement scales that have been designed to evaluate separately the various symptoms of neuropathic pain. QST allows an assessment of sensory detection thresholds for innocuous stimuli and pain thresholds, generally using the method of limits, less commonly the method of levels. It also includes the assessment of sensations induced by sub-threshold or suprathreshold stimuli, which may contribute to the identification and quantification of hyperalgesia. Finally, the chapter summarizes and discusses prior recommendations about the use of these measures in clinical trials.
This chapter describes commonly used peripheral nerve injury models of neuropathic pain. It introduces the central, non-traumatic and orofacial models of neuropathic pain. Neuropathic pain of central origin is observed clinically after traumatic incidents, such as stroke or spinal cord injury (SCI). An important consideration is that the pain experience, in humans and animals, has both sensory and emotional dimensions. The focus on nociception in pain research has been associated with the clinical failure of several potential pain medicines. An understanding of both sensory and affective dimensions of pain may improve translational research. Further, interpretations made from animal nerve injury models should be considered in the context of gender, age, and species/strain studied. Finally, it appears that no animal nerve injury model is without limitations, therefore, behavioral, physiological, and biochemical studies can only speculate on the relevance of experimental findings to human neuropathic pain.
Neuropathic pain after spinal cord injury (SCI) is a type of central neuropathic pain and is a frequent complication of spinal injury which is often refractory. Studies in animal models describe a number of peripheral and central pathophysiological processes after nerve injury that would be the basis of underlying neuropathic pain mechanisms. A major inhibitory system related to pain is opioid receptor mediated analgesia. In neuropathic pain, N-methyl-d-aspartate (NMDA) receptor activation increases excitation in the pain transmitting systems. Recent advances in pain research indicate multiple mechanisms, including many components of peripheral and central sensitization mechanisms, underlying the initiation and maintenance of neuropathic pain. Neurosurgical interventions may be treatment options in patients with poor pain control despite pharmacotherapy. Besides the effectiveness of a treatment, the adverse event profiles of these analgesics have to be considered before starting therapy or combining different agents.
This chapter explores the cellular and genetic mechanisms important in the development of neuropathic pain and other forms of chronic pain related to the phenomenon of sensitization. Peripheral sensitization contributes to pain hypersensitivity found at the location of tissue damage and/or inflammation. The chapter reviews the events that underlie pain as well as the anatomical and pharmacological basis for nociceptive sensations and chronic pain. Nociceptor excitation via various transient receptor potential (TRP) channels can result from a number of contributing processes. Transduction of mechanical, thermal, and chemical stimuli begins with membrane depolarization, which, if sufficient, transforms into an action potential. There are three classes of cell surface proteins at the sensory neuron important for sensory transduction: ion channels, metabotropic G protein-coupled receptors (GPCRs), and receptors for neurotrophins or cytokines. An important concept in central modulation of pain is the central inhibitory pathways and networks.
Over the past 150 years, regional post-traumatic pain has had various appellations, most recently complex regional pain syndrome (CRPS) and post-traumatic neuralgia (PTN). CPRS appears to be a complex endophenotype of PTN that involves neurogenic inflammation as well as pain. There is increasing evidence that peripheral and central inflammatory cascades triggered by nerve injuries contribute to CRPS and perhaps PTN as well. PTN and CRPS often spread beyond classic individual nerve territories, although when patients are asked to outline the epicenter, or most abnormal area, this frequently identifies a specific nerve injury. The most dramatic CRPS and PTN-associated movement abnormality is fixed distal dystonia. Nerve conduction studies and electromyography are useful in documenting and localizing peripheral nerve damage. Currently, four classes of medications are primary options for chronic CRPS/PTN: tricyclics and serotonin-noradrenaline reuptake inhibitors; opioids; gabapentinoids; and topical or systemic local anesthetics.