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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The headache phase of migraine may develop as the result of an abnormal interaction (and perhaps an abnormal release) of vasoactive neurotransmitters from terminals of the trigeminal nerve with large intracranial and extracranial blood-vessels. These blood-vessels, which dilate during the headache phase of migraine, are thought to receive axonal projections from all three divisions of the trigeminal nerve. Substance P, a potent vasodilating peptide, seems to be released from trigeminal nerve endings in response to nervous stimulation and is involved in the transmission of painful stimuli within the periphery. The vasoactive molecule serotonin, implicated in the pathogenesis of migraine, coexists with substance P in some terminals of the central nervous system and is present within the trigeminal ganglia. Within this nerve serotonin may modulate the function of primary sensory neurons. The abnormal release of substance P or as yet unidentified peptides or other transmitters from the fifth cranial nerve may explain both the hemicranial pain and the vasodilation which are characteristic of the headache of migraine.
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PMID:Neurotransmitters and the fifth cranial nerve: is there a relation to the headache phase of migraine? 9 Sep 71

We report the first known case of daunorubicin administered directly into the human central nervous system. A 3 1/2-year-old female with pneumonia and otitis media was diagnosed with acute lymphoblastic leukemia and was admitted for antibiotics and chemotherapy. On the first day she inadvertently received a 17 mg intrathecal (IT) injection of daunorubicin. When the error was recognized about 1 hour later, her cerebrospinal fluid (CSF) was exchanged with sterile saline by barbotage, IT hydrocortisone was given, a subarachnoid catheter was inserted, and the CSF was allowed to drain for 36 hours. Only 5.6 mg (33%) of the dose was recovered from CSF, 2.7 mg as daunorubicin and 2.9 mg as the metabolite, daunorubicinol. Initially she was asymptomatic and induction therapy continued with vincristine, 1-asparaginase, prednisone, and IT methotrexate. One week after the daunorubicin injection she developed headache and irritability; CSF protein was 3.2 gm/dl. On the 12th day, she developed fungal sepsis and worsening pneumonia. On the 15th day, she became comatose with a flacid paraparesis, areflexia, and an ascending progressive bulbar palsy. A series of computerized tomography scans over 6 weeks showed increasing diffuse cerebral atrophy. Nerve conduction velocity studies were consistent with an axonal neuropathy. Despite her multiple concurrent medical problems, the timing and characteristics of neurologic damage suggest that IT daunorubicin caused progressive destruction of the nervous system.
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PMID:Inadvertent intrathecal injection of daunorubicin with fatal outcome. 157 39

We present a 66-year old woman suffering from a chronic disorder characterized by multiple paroxysmal symptoms precipitated by coughing. These included cephalalgia, syncope, binocular photopsia phenomena with blurred vision, and an "electric-like" paroxysmal tingling of the hands. In addition to a central spinal cord cavity and hindbrain herniation, magnetic resonance imaging showed multiple skeletal anomalies and the craniospinal junction which included a narrow clivo-axial angle, basilar impression of the skull and a tight foramen magnum. Resonance magnetic imaging showed a high-signal intensity lesion on T2-weighted images at the posterior medullo-spinal junction suggesting focal demyelination. We propose that paroxysmal symptoms induced by coughing in patients bearing hindbrain ectopia and skeletal anomalies at the foramen magnum region may involve different pathogenetic mechanisms, including ectopic axonal activity and ephaptic transmission at the sensory pathways. This caused a Lhermitte-like phenomenon precipitated by coughing, rather than by forward flexion of the neck. However, increased pressure at the posterior fossa presumably underlies all these phenomena, and may therefore be potentially relieved by suboccipital decompressive craniotomy.
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PMID:[Arnold-Chiari malformation with multiple paroxysmal manifestations induced by coughing]. 845 93

Hematomas of the basal ganglia in head injury have long been recognized by pathologists with an interest in head injury but their mechanism has not been revealed clearly. We report two cases of bilateral traumatic hemorrhage in the basal ganglia. Case #1, a 17-year-old male was admitted to our hospital immediately after a traffic accident. Neurological examination revealed that the patient was comatose and had right hemiparesis. CT scan showed bilateral hemorrhage of the basal ganglia and subarachnoid hemorrhage in the perimesencephalic cistern. MRI showed high signal intensity areas in the bilateral basal ganglia, perimesencephalic cistern, cerebral white matter and corpus callosum. The patient was diagnosed as having diffuse axonal injury coinciding with bilateral hemorrhage of the basal ganglia. Stereotactic aspiration for the hematoma of the left basal ganglia was carried out. Case #2, a 75-year-old male was admitted immediately after falling from the roof of his house. Neurological examination revealed no neurological deficit except for headache and nausea. CT scan on the day of injury revealed no abnormality. But CT scan 12 hours following the injury showed bilateral hemorrhage of the basal ganglia. Blood pressure of the patient was within normal range and he was diagnosed as having traumatic bilateral intracerebral hematoma. Conservative treatment was carried out and the patient was discharged 7 days after injury with no neurological deficit. The mechanism of traumatic hemorrhage of the basal ganglia has not been clear. In case #1, diffuse axonal injury (DAI) may have played an important role in the bilateral hemorrhage. But in case #2, non-DAI factor such as vasoparalysis syndrome may have existed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral traumatic hemorrhage in the basal ganglia: report of two cases]. 204 52

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82

Renal failure and its treatment are associated with a number of neurologic complications that must be differentiated from the nervous system complications of the disease leading to renal failure. Uremic encephalopathy is characterized by clinical signs of depressed brain function coexisting with excitation, often in the form of generalized epileptic seizures. Peripheral neuropathy, due to axonal involvement, is common and is characterized by ascending sensory and motor dysfunction. The treatment of renal failure also may lead to the development of neurologic abnormalities in the form of dialysis disequilibrium characterized by headache, nausea, irritability that may progress to seizures, coma, and death, which is caused by the entry of free water into the brain and swelling. Dialysis dementia, caused by the toxic effects of aluminum, is now rare. Renal transplant recipients may develop cerebrovascular disease, infections by opportunistic organisms, or malignant neoplasms, particularly primary lymphoma of the brain. As transplant recipients live longer and more operations are performed, additional complications may be seen in the future.
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PMID:Neurologic complications of renal disease. 254 62

Trauma to the head and neck can cause minor head injury with a brief alteration in consciousness. Generally, neurologic examination yields normal findings. In some patients, however, postconcussion syndrome marked by headache, dizziness, and neuropsychological deficits (eg, fatigue, cognitive impairment, emotional symptoms) results. This acceleration-deceleration injury with cerebral axonal dysfunction is an organic disease having objective abnormalities that necessitate early neurologic testing and treatment to prevent serious complications.
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PMID:Minor head injury may not be 'minor'. 265 25

The trigeminal sensory innervation of the major cerebral vessels is thought to carry the nociceptive information during a migraine headache, and this pain is usually referred to the forehead area. Using retrograde tracing techniques, we have described the distribution of sensory trigeminal cells that innervate the middle cerebral artery (MCA) and the forehead. Nearest-neighbor analysis of the ophthalmic division of the trigeminal ganglion revealed that cells innervating the forehead tend to be clumped around individual cells that innervate the MCA. An average of less than 1 cell per animal was found to project divergent collaterals to both areas. The close association of ganglion cell bodies innervating the cerebral vasculature and those innervating forehead areas may underlie the convergence of their central processes onto common brain-stem trigeminal nucleus cells, and thus the referral of headache pain. In contrast to the lack of ganglion cells with axonal collaterals to the cerebral vasculature and forehead, a significant population of cells that innervate the MCA also have collateral projections to other cerebral arterial branches (branches of the middle meningeal artery), as well as the surrounding dura. Thus, the innervation targets of individual trigeminal cells are very widespread intracranially (including arteries and dura), but separate cells in the ophthalmic division innervate extracranial targets.
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PMID:Pattern of intracranial and extracranial projections of trigeminal ganglion cells. 348 82

The pathology of mild head injury, its common behavioral sequelae, the nature of the recovery process, and the psychosocial consequences are reviewed. Acceleration-deceleration head trauma, causing brief unconsciousness, and leaving no frank neurological deficit, is associated in primates with axonal and terminal degenerative changes in brain stem nuclei. Although the presence of clinical demonstrable neurological abnormality increases the likelihood of subsequent deficits, their absence does not guarantee full recovery. Among mildly injured children, the relationships between persistent behavioral deficits and their age of onset correspond closely with those observed in children with overt damage, making it unlikely that psychological-behavioral deficits are attributable to non-neurological aspects of the injury. Deficits observed include distractability, irritability, headaches, inability to maintain a prior level of cognitive competence, and impulsivity. Although longer periods of unconsciousness are associated with permanent memory deficits, minimal unconsciousness is also followed by consistent deficits in complex memory tasks. Detailed neuropsychological testing of mildly injured children has revealed persisting deficits even after 5 years. Furthermore, deficits arising from repeated injuries are cumulative. The importance of adequate neuropsychological assessment and accurate information to the patient are stressed as important in helping satisfactory adjustment.
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PMID:Mild head injury. 636 11

A case of 38 year old man who worked with organochlorinated and Parathion during 5 years is reported. His follow-up was up to 2 years. The onset of the disease was characterized by cholinergic signs, headache, loss of weight, trembling, miokimias, fasciculations, ataxia, myotonic phenomena (in hands only) and motor sensitive peripheral polyneuropathy (affecting the lower limbs symmetrically). Low concentrations of blood cholinesterases confirmed the etiology. Myotonic phenomena disappeared spontaneously 6 months after the initial observation. One year later, the concentration of erythrocyte acetylcholinesterase was found to be low and plasma cholinesterase was normal, suggesting that the patient was carrier of a congenital deficiency of acetylcholinesterase. In literature relationship between myotonia and intoxication due to organophosphorus was not found. The whole clinical picture, cholinergic symptoms, transitory phenomena and spontaneous motor activity could be explained by an excess of acetylcholine. Electromyography (EMG) in the first observation showed neuromuscular transmission blocking characterized by deficiency or absence of voluntary activity, unexcitability of fibular nerves, with fibrillations and positive peaks as described previously with Mipafox (another organophosphorus agent). During 2 years of observation numerous end-plates potentials of muscular fibres persisted in the EMG. A progressive increase in voluntary activity showed by unit motor potential of almost normal amplitude and very increased duration was observed. No potentials of reinnervation were noted. The results of EMG were explained as disturbances of neuromuscular transmission associated with moderate signs of denervation. The Eaton-Lambert's test and the stimulation of a single unit motor potential confirmed disorder of neuromuscular synapses. The histochemistry of brachial biceps showed scattered atrophic and angulated type I and II fibres. Teased-fibres preparations showed nerve fibres with B, C, and G alterations as defined by Dyck et al. indicating axonal degeneration. These results were according to velocity of sensitive conduction. The conduction velocity of fibular nerves was strongly delayed during all the evolution indicating serious disorders of motor nerves myelin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Polyneuropathy caused by parathion: clinical, electrophysiologic and histologic studies of a case]. 665 78


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