Since the earliest descriptions of pain related to injury of the nervous system, it has been recognized that the characteristics of this type of pain differ markedly from those of pain due to nonneural tissue damage. Later as new analgesics were developed, it became clear that neurogenic pain was very often refractory to these drugs. Recently neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system." Inflammatory reaction and neuropathic pain are often considered to be distinct entities. The development of neuropathic pain involves not only neuron but also inflammatory cells, chemokines, and glial cells. Treatment of neuropathic pain is difficult and frequently unrewarding. The basic principles are (1)the identification and elimination of the underlying pathologic mechanism that maintains central sensitization; (2)the use of nonsteroidal anti-inflammatory drugs to reduce peripheral sensitization and modulate the activity of nociceptors; (3)the use of tricyclic antidepressants to induce sleep and decrease lancinating and burning neuropathic pain; (4)a trial of gabapentin, pregabalin, lamotrigine and topamax; (5)the use of lidocaine patch for intractable trigeminal neuralgia; (6)sympathetic blockade for complex regional pain syndrome while patients are stick sympathetically maintained; (7)dorsal column stimulation; (8)intrathecal therapies including morphine, clonidine, and GABAB agonists when other less invasive therapies have failed. In this article we reviewed the role of peripheral inflammation for development of neuropathic pain, diagnosis, and new opportunities for treatment of neuropathic pain, especially focused on medical treatments with antiepileptics and antidepressants.
Amines ; Analgesics ; Anticonvulsants ; Antidepressive Agents, Tricyclic ; Burns ; Chemokines ; Clonidine ; Cyclohexanecarboxylic Acids ; gamma-Aminobutyric Acid ; Humans ; Inflammation ; Lidocaine ; Morphine ; Nervous System ; Neuralgia ; Neuroglia ; Neurons ; Pregabalin ; Triazines

Claude syndrome is a well known midbrain syndrome which is characterized by ipsilateral oculomotor nerve palsy and contralateral cerebellar ataxia by the lesion of the red nucleus. Although this syndrome was reported as early as in 1924 by Claude, only a few cases have been reported. Moreover, the midbrain infarction as a cause of Claude syndrome has quite rarely been described. Firstly, we report a 61-year-old patient with partial oculomotor nerve palsy and contralateral cerebellar ataxia who demonstrated an infarction just caudal to the red nucleus on MRI. Secondly, we also discuss the probable vertical fascicular arrangement of the oculomotor nerve in the midbrain.
Brain Stem Infarctions* ; Cerebellar Ataxia ; Humans ; Infarction ; Magnetic Resonance Imaging ; Mesencephalon* ; Middle Aged ; Oculomotor Nerve ; Oculomotor Nerve Diseases ; Red Nucleus

BACKGROUND AND PURPOSE: The World Health Organization (WHO) has classified thymic carcinoma and other thymomas (types A, AB, and B) as different neoplasms. Myasthenia gravis (MG) is an early sign of thymoma and theoretically does not accompany thymic carcinoma; however, cases of thymic carcinoma with MG have been reported. Whether thymic carcinoma can accompany MG has yet to be established. METHODS: The medical records of patients who underwent thymectomy for MG between 1990 and 2011 in a single hospital were reviewed. All cases with the diagnostic code of "thymic carcinoma" or "thymoma type C" (old terminology) were selected. A pathologist re-reviewed the pathologic specimens using the new WHO criteria. The rate of thymic carcinoma among these MG patients was then calculated. RESULTS: A total of 81 patients with MG had thymic tumors, 10 of whom had thymic carcinomas or thymoma type C. Seven cases of well-differentiated thymic carcinomas (type B3) were excluded, leaving three (3.7%) cases of thymic carcinoma with MG. All three of these cases were type B3 thymoma with a focal squamous cell carcinoma component that was very small and well demarcated. In addition, two out of the three tumors were found to be at an early clinical stage. All of the cases survived without recurrence over follow-up periods of at least 5 years. CONCLUSIONS: Thymic carcinoma transformation from thymoma can occur during the early stages of thymoma. The association of this condition with MG is not as rare as was previously thought. Thymic carcinomas accompanying MG had a predominant B3 thymoma component with a focal thymic carcinoma area (squamous cell carcinoma).
Carcinoma, Squamous Cell ; Follow-Up Studies ; Humans ; Medical Records ; Myasthenia Gravis* ; Recurrence ; Thymectomy ; Thymoma* ; Thymus Neoplasms ; World Health Organization

Hyperperfusion syndrome (HS) is characterized by unilateral headache, seizures, and hypertension and may result in intracerebral hemorrhage. HS is a serious complication following carotid endarterectomy or angioplasty, but it is rarely reported after evacuation of chronic subdural hematoma (CSH). A 75-year-old man developed headache, seizure, and hemiparesis after evacuation of CSH. HS is diagnosed by a postoperative transcranial Doppler. His symptoms subsided with anti-hypertensive medications. Early recognition of this syndrome may be important in reducing postoperative morbidity of CSH.
Aged ; Angioplasty ; Cerebral Hemorrhage ; Endarterectomy, Carotid ; Headache ; Hematoma, Subdural, Chronic* ; Humans ; Hypertension ; Paresis ; Seizures

No abstract available.
Ciguatoxins ; Eating* ; Intestines* ; Marine Toxins ; Neurologic Manifestations* ; Quadriplegia

No abstract available.
Brain Stem* ; Hyperthyroidism* ; Spinocerebellar Degenerations*

PURPOSE: Subacute combined degeneration (SCD) involves progressive degeneration of the spinal cord, optic nerve, and peripheral nerves. Vitamin B12 (VB12) is a co-factor in myelin synthesis. Because each cell that constitutes the myelin component in the central nervous system and peripheral nervous system is different, it is improbable that these cells undergo simultaneous degeneration. However, the sequence of degeneration in SCD has not been established. MATERIALS AND METHODS: In this study, we analysed medical records and electrophysiological data of patients who showed neurological symptoms and whose serum VB12 levels were lower than 200 pg/mL. RESULTS: We enrolled 49 patients in this study. Their mean VB12 level was 68.3 pg/mL. Somatosensory evoked potential (SEP) study showed abnormal findings in 38 patients. Of the 40 patients who underwent visual evoked potential (VEP) study, 14 showed abnormal responses. Eighteen patients showed abnormal findings on a nerve conduction study (NCS). In this study, abnormal posterior tibial nerve SEPs only were seen in 16 patients, median nerve SEPs only were seen in 3 patients, abnormal VEPs only in two, and abnormal NCS responses in one patient. No patient complained of cognitive symptoms. CONCLUSION: In SCD, degeneration appears to progress in the following order: lower spinal cord, cervical spinal cord, peripheral nerve/optic nerve, and finally, the brain.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Evoked Potentials, Somatosensory/physiology ; Female ; Humans ; Male ; Middle Aged ; Subacute Combined Degeneration/*blood/metabolism/*physiopathology ; Vitamin B 12/blood ; Vitamin B 12 Deficiency/blood/complications ; Young Adult

Cerebral malaria is a severe neurological complication of Plasmodium falciparum infection. Cerebral malaria can lead to cerebral infarction by several mechanisms including systemic inflammatory response. The systemic inflammatory response is known to rarely occur in Plasmodium vivax infection. We report a patient who developed multiple cerebral infarctions following Plasmodium vivax infection.
Cerebral Infarction ; Humans ; Malaria, Cerebral ; Plasmodium ; Plasmodium falciparum ; Plasmodium vivax

Delayed-onset continuous bruxism due to brain stem infarction has not yet been reported. A 49-year old man presented with quadriplegia and ophthalmoplegia. Brain MRI showed acute infarction in the bilateral midbrain, right thalamus and the superior cerebellum. One month later, the patient developed bruxism which persisted during sleep. A palatal myoclonus was not observed. Follow up MRI taken 4 months later showed bilateral olivary hypertrophy. We suggest that the patient's bruxism may be related to the olivary hypertrophy. The bruxism generator may be located in the pontine-reticular-formation (PRF). Bilateral large midbrain lesions interrupting the cortical inhibition may have produced bilateral olivary hypertrophy, which could stimulate the PRF, producing continuous bruxism.
Brain ; Brain Stem Infarctions* ; Bruxism* ; Cerebellum ; Follow-Up Studies ; Humans ; Hypertrophy* ; Infarction ; Magnetic Resonance Imaging ; Mesencephalon ; Middle Aged ; Myoclonus ; Ophthalmoplegia ; Quadriplegia ; Thalamus

No abstract available.
Marchiafava-Bignami Disease* ; Thalamus