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

We describe a patient with abnormal ocular movement, probably due to dysfunction of saccade generation mechanism in the lower pons involving the omnipause neuron and a feed-back circuit. A 26-year-old man had fever, mild headache and sore throat for a few days and also noted unstable gait and diplopia. These symptoms subsided, but he noticed oscillopsia about 2 months later. On admission in our hospital, the neurological examination revealed no abnormalities except for abnormal eye movements, which were induced by voluntary or involuntary ocular movement and lasted for a few minutes. The abnormal ocular movement was irregular in direction, amplitude and rhythmicity, and the voluntary and involuntary ocular movements could not be elicited during the period of this abnormal ocular movement. The abnormal ocular movement completely disappeared for about 1 hour by intravenous injection of TRH. At this time bilateral mild abducens palsy was demonstrated by EOG examination. The abnormal ocular movement in this patient, which has nerve been reported in the literature, was considered to be due to a disinhibition of excitatory burst neuron (EBN) caused by the dysfunction of omnipause neuron, and possibly due to a delay of feed-back information of saccade to the EBN.
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PMID:[Unusual pathological ocular movement caused by dysfunction of the saccade generation mechanism]. 142 43

The authors observed children aged 1 to 7 years without any signs of epilepsy in the anamnesis. The children were examined for headaches, memory deterioration, difficulties in the learning, some types of tics, stammering, and psychomotor disinhibition. Among them, a group of 35 children characterized by specific movements of the eye balls as was shown by estimation of oculomotor nerve functions (look anxiety, "falling look") were distinguished. EEG examinations discovered the peak-wave type complexes related to the signs of petit mal of the absence type. The conclusion is a precursor of paroxysmal conditions. It is recommended that adequate anticonvulsive therapy be initiated provided the symptom is identified together with the EEG changes.
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PMID:["Falling look" symptom in the structure of the neurological status as a precursor of paroxysmal conditions in young children]. 178 95

An hypothesis regarding the possible role of the carotid body in the pathogenesis of cluster headache is presented. It states: 1. The pathways concerned with cyclic cluster periods may begin centrally involving specific areas in the hypothalamus. The major influence of this physiological change is proposed to be an inhibition of the sympathetic and disinhibition of parasympathetic supplies to the carotid body. The result, whether due to increased vasomotor tonus or interruption of intrinsic sympathetic stimulation, is suggested to cause diminished peripheral chemoreceptor activity. 2. The pathway concerned with onset of spontaneous or induced attacks begins, as proposed, with oxygen desaturation--which, upon reaching threshold levels may induce a hyperactive chemoreceptor response, and stimulate through afferent pathways the nuclei of the 7th and 10th cranial nerves and respiratory centers, via the nucleus solitarius. 3. The consequence of this excitation may involve the third suggested pathway resulting in stimulation of peripheral secretory and other receptors innervated by the cranial nerves.
Cephalalgia 1983 Dec
PMID:A possible role of the carotid body in the pathogenesis of cluster headache. 664 Jun 58

Headache is a vast field with many different varieties of headaches and classifications. However, all headaches have a common anatomy and physiology. All headaches are mediated by the trigeminocervical nucleus, and are initiated by noxious stimulation of the endings of the nerves that synapse on this nucleus, by irritation of the nerves themselves, or by disinhibition of the nucleus. A mastery of the relevant anatomy and physiology of the trigeminocervical nociceptive system serves to predict and summarise the many varieties of headache systematically and with reference to their mechanisms.
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PMID:Anatomy and physiology of headache. 874 69

meta-Chlorophenylpiperazine (mCPP) is a compound that is frequently used in challenge tests of the serotonergic system. Its human pharmacology is largely unexplored. The objective of this study was to investigate the pharmacokinetic and pharmacodynamic profile of mCPP. Eight female and six male healthy volunteers were included in a randomized, double-blind, double-dummy, three-way crossover design of single-dose intravenous (0.1 mg/kg), oral (0.5 mg/kg), and placebo treatment, with 24-hour follow-up. mCPP showed a large variability in clearance (11-92 mL/hr) and bioavailability (14-108%). Two female subjects dropped out because of headache and dysphoria. During the 27 occasions in which mCPP was administered, autonomic physical symptoms were observed in 23 subjects and disturbances of mood in 6 subjects. Oral and intravenous mCPP caused sudden increases in cortisol levels, prolactin levels, and total scores of the Body Sensation Questionnaire. Administration of mCPP also led to concentration-dependent increases of saccadic peak velocity and adaptive tracking performance and to a decrease of electroencephalographic occipital theta activity. No clinically relevant effects on electrocardiogram, temperature, and blood pressure were found. In conclusion, it is doubtful whether mCPP is a useful compound for challenge tests in view of the large pharmacokinetic variability after intravenous and oral administration. The effects of mCPP are consistent with disinhibition of the central nervous system.
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PMID:Pharmacokinetic and pharmacodynamic profile of oral and intravenous meta-chlorophenylpiperazine in healthy volunteers. 969 Jun 94

Migraine sufferers have abnormal cerebral information processing and personality disorders, post-traumatic headache sufferers also have some personality changes. We therefore, studied intensity dependence of auditory evoked potentials, Plutchik-van Praag's depression inventory, Zuckerman's sensation seeking scales and Zuckerman-Kuhlman's personality questionnaire in patients suffering from migraine without aura (n = 26) and chronic post-traumatic headaches (n = 26) as well as in healthy volunteers (n = 30). The migraine group showed significantly increased neuroticism-anxiety than controls, increased intensity dependence of N1-P2, and decreased thrill and adventure score compared with the controls and post-traumatic headaches. The post-traumatic headache had significantly increased depression compared with the controls, and increased disinhibition compared with the controls and migraines. This study demonstrates that the two headache types have different neurophysiological and personality traits. The pronounced intensity dependence of N1-P2 suggests a cortical potentiation response, together with a decreased thrill and adventure seeking, favor a lower serotonergic innervation in migraine. While the elevated disinhibition and depression, as consequences, may be linked with the wide cortical neuronal/axonal degeneration in post-traumatic headache.
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PMID:Auditory evoked potentials and multiple personality measures in migraine and post-traumatic headaches. 1006 69

SUNCT (Shortlasting Unilateral Neuralgiform Headache attacks with Conjunctival injection and Tearing) is a syndrome characterised by shortlived (5-240 s), strictly unilateral, orbital/periorbital, moderate-to-severe pain attacks, accompanied by rapidly developing conjunctival injection and lacrimation. Most attacks are triggered by mechanical stimuli, but there are also spontaneous attacks. Symptomatic periods alternate with remissions in an unpredictable fashion. In active periods, the attacks predominate during daytime, with a frequency that ranges from < 1 attack/day to > 30 attacks/h SUNCT is mainly a primary disorder, but is sometimes associated with intracranial structural lesions (symptomatic SUNCT). SUNCT has been included in the group of trigeminal autonomic cephalalgias, which are thought to depend on the activation of the trigeminal system together with the disinhibition of a trigeminofacial autonomic reflex. According to a few reports, SUNCT patients may benefit from carbamazepine, lamotrigine, gabapentin, topiramate or various surgical procedures. However, well-designed clinical trials are required before these therapeutic options can be sufficiently validated.
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PMID:SUNCT syndrome: an update. 1593 85

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a new category of treatment-responsive encephalitis associated with "anti-NMDAR antibodies", which are antibodies to the NR1/NR2 heteromers of NMDAR. The antibodies are detected in the CSF/serum of young women with ovarian teratoma, who typically develop schizophrenia-like psychiatric symptoms, usually preceded by fever, headache, or viral infection-like illness. After reaching the peak of psychosis, most patients developed seizures followed by an unresponsive/catatonic state, decreased level of consciousness, central hypoventilation frequently requiring mechanical ventilation, orofacial-limb dyskinesias, and autonomic symptoms. Brain MRI is usually unremarkable but focal enhancement or medial temporal lobe abnormalities can be observed. The CSF reveals nonspecific changes. EEG often reveals diffuse delta slowing without paroxysmal discharges, despite frequent bouts of seizures. This is a highly characteristic syndrome evolving in 5 stages, namely, the prodromal phase, psychotic phase, unresponsive phase, hyperkinetic phase, and gradual recovery phase. The hyperkinetic phase is the most prolonged and crucial. This disorder is usually severe and can be fatal, but it is potentially reversible. Once patients overcome the hyperkinetic phase, gradual improvement is expected with in months and full recovery can also be expected over 3 or more years. Ovarian teratoma-associated limbic encephalitis (OTLE) was first reported in 1997 when this syndrome was reported independently in 1 Japanese girl and 1 woman, both of whom improved following tumor resection. In 2005, Dalmau and his research group first demonstrated antibodies to novel neuronal cell membrane antigens in 4 women with OTLE in a non-permeabilized culture of hippocampal neurons. Two years later, they identified conformal extracellular epitopes present in the NR1/NR2B heteromers of NMDAR, which are expressed in the hippocampus/forebrain. The target extracellular epitopes are not detectable by immunoblotting, and should not be confused with the linear epitopes of NR2B subunits (also known as epsilon2). The antibodies disappear with clinical improvement, suggesting their pathogenic role. Autopsies revealed IgG deposits in the hippocampus, extensive microgliosis, rare T-cell infiltrates, and neuronal degeneration predominantly involving, but not restricted to, the hippocampus. The nervous tissues of the tumors exhibit not only strong expression of the NR2B subunits but also reactivity with the patients' antibodies. The pathogenesis remains unknown; however, this disorder is considered to be an antibody-mediated encephalitis. Based on the current NMDAR hypofunction hypothesis of schizophrenia, we speculate that the antibodies may cause inhibition rather than stimulation of NMDARs in presynaptic GABAergic interneurons, causing a reduction in GABA release. This results in disinhibition of postsynaptic glutamatergic transmission, excessive release of glutamate in the prefrontal/subcortical structures, and glutamate and dopamine dysregulation that might contribute to development of schizophrenia-like psychosis and bizarre dyskinesias. The antibodies were initially found only in young women with teratoma in the ovaries. However, recent studies show that this disorder can occur even in the absence of teratoma in up to 35% of patients, and even boys and adult men had been affected. Although recovery occurs without the need for tumor removal, the severity and extended duration of symptoms support tumor removal. Combined therapy including tumor resection and immunotherapy is recommended. In this review, we also discuss the relationship between anti-NMDAR encephalitis and related disorders, including acute diffuse lymphocytic meningoencephalitis and acute juvenile female non-herpetic encephalitis (AJFNHE).
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PMID:[Anti-nMDA receptor encephalitis--clinical manifestations and pathophysiology]. 1880 39

Cluster headache (CH) is a neurovascular headache disease characterized by recurrent, strictly unilateral, severe pain attacks. Despite its typical clinical features, including circadian rhythm of the attacks and ipsilateral autonomic dysfunction, the underlying pathophysiology of CH is still unclear. Electrophysiological data point to central disinhibition of the trigeminal nociceptive system as one of the key mechanisms of CH pain. Therefore, altered habituation pattern and changes within trigeminal-facial neuronal circuits due to central sensitization seem to be involved. One biochemical correlate is probably represented in dysfunctions of serotonergic raphe nuclei-hypothalamic pathways. Structural and functional imaging data show an alteration of hypothalamic structures in CH patients, supporting the hypothesis that the hypothalamus, according to its function as a circadian pacemaker, plays a pivotal role in CH pathology. Cortical and brainstem reflexes are reviewed to illuminate the pathophysiology of CH.
Curr Pain Headache Rep 2009 Apr
PMID:The electrophysiology of cluster headache. 1927 82

Migraine is a common episodic headache disorder characterized by attacks that consist of various combinations of headache and neurologic, gastrointestinal and autonomic symptoms. Migraine with aura may be due to neuronal hyperexcitability, perhaps from cortical disinhibition. It is likely that headache results from the activation of meningeal and blood vessel nociceptors combined with a change in central pain modulation. Antiepileptic drugs are increasingly being recommended for migraine prevention since placebo-controlled, double-blind trials prove them to be effective. Topiramate is a structurally unique antiepileptic drug that was discovered by serendipity. It is a derivative of the naturally occurring monosaccharide D-fructose and contains sulfamate functionality. Topiramate may bind to membrane channel complexes at phosphorylation sites in the inner loop and, thereby, allosterically modulate ionic conductance through the channels. The topiramate MIGR-001, MIGR-002 and MIGR-003 trials represent the largest controlled trials of a migraine preventive agent ever performed. Treatment with 100 or 200 mg/day of topiramate was associated with significant reductions in migraine frequency, migraine days and the number of migraine attacks per month. Topiramate was also associated with a reduced use of acute medications. The most common adverse events were difficulty with concentration and attention, difficulty with memory, mood problems, anorexia and weight loss, paresthesias, hypoesthesia and language problems. Topiramate is a first-line migraine preventive drug and should be considered preferentially for all patients in whom weight gain is a concern, who are currently overweight or who have coexistent epilepsy or bipolar disease.
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PMID:Topiramate in migraine prevention. 1981 Aug 79


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