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

Trigeminal nerves provide the principal afferent pathways for the transmission of intracranial and extracranial head pain. This study, using two retrograde axonal tracers, demonstrated that first division afferents projecting to intracranial and extracranial targets are not commonly axon collaterals of the same neuron. Therefore, divergent axon collaterals probably are not responsible for the phenomenon of referred pain within the first trigeminal division.
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PMID:Do intracranial and extracranial trigeminal afferents represent divergent axon collaterals? 684 99

The Toxic Syndrome (TS) caused by ingestion of adulterated rapeseed oil in Spain is a new disease of multisystemic character whose aetiology and pathogenesis remains unknown. The most prominent pathological feature is a peculiar non-necrotizing vasculitis, that affects mainly the intima and involves vessels of every type and size in practically every organ. The TS begins with an acute clinical picture with pleuropneumopathy, fever, headaches, exanthems and eosinophilia. In these early clinical phases the main pathological findings were observed in the lungs and consisted of intense pulmonary interstitial oedema with scanty inflammatory mononuclear infiltrates. Ultrastructural study revealed hydropic degeneration of pneumocytes types I and II with desquamation of type I. The patients in this phase died of respiratory failure, later deaths were due to thromboembolic complications. Later still the patients developed a neuromuscular syndrome, sclerodermiform skin lesions and severe weight loss and died predominantly of infectious complications and respiratory failure. The anatomopathological picture in the peripheral nerves was that of inflammatory neuropathy with a lymphocytic perineuritis that led to perineural fibrosis with secondary axonal degeneration. The muscle presented an interstitial inflammatory myopathy at first followed by a neurogenic muscular atrophy. The skin lesions in the late phases consisted in dermal or dermal and subdermal fibrosclerosis, with vasculitis of the small arteries in the lower dermis. The salivary glands and pancreas showed vasculitis and interstitial inflammation which progressed to interstitial fibrosis and parenchymal atrophy.
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PMID:Pathology of a new toxic syndrome caused by ingestion of adulterated oil in Spain. 715 66

The skin of both temples was examined ultrastructurally in six patients with cluster headaches and in three controls. An increased number of mast cells were present in the patients irrespective of whether they were in a cluster period or in a quiescent phase. The mast cells were found perivascularly and in the vicinity of cutaneous nerves in the patients, whereas they were predominantly found in perivascular areas in controls. Mast cell degranulation was not more prominent on the side of the pain and occasional degranulated mast cells were found in controls. These findings are consistent with the hypothesis that cluster headache is due to an axonal reflex in the trigeminal system, initiated perhaps by latent viral infection of IgE activation of mast cells.
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PMID:Cluster headache. Ultrastructural aspects and pathogenetic mechanisms. 722 18

A 37-year-old woman with complaints of headache and nausea presented with temporary disturbance of consciousness, bulbar palsy and ataxic speech following flu-like symptoms. After the recovery of her consciousness, she developed orthostatic syncope and numbness all over the body. When she was admitted to our hospital two months later, she showed emaciation, diminished sweat production and butterfly-patch-like pigmentation. Neurologic examinations were remarkable for anisocoric pupils that sluggishly reacted to light, impaired left facial movements, bulbar palsy, numbness of the whole body, total loss of all tendon reflexes, incordination, ataxic gait and severe postural hypotension. Laboratory data included albuminocytogenic dissociation in cerebrospinal fluid, convergence nystagmus and dysmetria in electronystagmography, and right trigeminal paralysis in blink reflex. A sural nerve biopsy showed active axonal degeneration and severe loss of both myelinated and unmyelinated fibers. Examinations of autonomic nervous system disclosed diffuse impairment of sympathetic and parasympathetic postganglionic nerve. Based on these findings she was diagnosed as having acute pandysautonomia. High titer of serum EB virus antibody suggested that acute pandysautonomia and diffuse brainstem impairment may be related to EB virus infection.
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PMID:[A case of acute pandysautonomia and diffuse brain stem impairment associated with EB virus infection]. 772 95

1. The effects of an intravenously administered sumatriptan analogue were examined on c-fos-like immunoreactivity (c-fos-LI), a marker of neuronal activation, evoked within trigeminal nucleus caudalis (TNC) and other brain stem regions 2 h after intracisternal injection of the irritant, capsaicin (0.1 ml, 0.1 mM), in pentobarbitone-anaesthetized Hartley guinea-pigs. 2. C-fos-LI was assessed in eighteen serial sections (50 microns) using a polyclonal antiserum. A weighted average, reflecting total expression within lamina I, IIo of TNC was obtained from three representative levels (i.e., at -0.225 mm, -2.475 mm and -6.975 mm.). 3. Capsaicin caused significant labelling within lamina I, IIo, a region containing axonal terminations of small unmyelinated C-fibres, as well as within the nucleus of the solitary tract, area postrema and medial reticular nucleus. A similar distribution of positive cells was reported previously after intracisternal injection of other chemical irritants such as autologous blood or carrageenin. 4. Pretreatment with a conformationally restricted sumatriptan analogue (with some selectivity for 5-HT1B and 5-HTID receptor subtypes) CP-122,288, reduced the weighted average by approximately 50-60% (P < 0.05) in lamina I, IIo at > or = 100 pmol kg-1, i.v., but did not decrease cell number within area postrema, nucleus of the solitary tract or medial reticular nucleus. A similar pattern was reported previously following sumatriptan, dihydroergotamine or CP-93,129 administration after noxious meningeal stimulation. 5. We conclude that modifications at the amino-ethyl side chain of sumatriptan dramatically enhance the suppression of c-fos expression within TNC, a finding consistent with its remarkable potency against neurogenic plasma protein extravasation within dura mater. CP-122,288 and related analogues may serve as an important prototype for drug development in migraine and related headaches.
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PMID:Suppression by the sumatriptan analogue, CP-122,288 of c-fos immunoreactivity in trigeminal nucleus caudalis induced by intracisternal capsaicin. 778 Jun 55

Single unit recording studies in anesthetized cats have identified a population of neurons in the brainstem trigeminal complex that can be activated by stimulation of major dural blood vessels. Such dura-responsive neurons exhibit response properties that are appropriate for a role in the mediation of vascular head pain in that they typically exhibit nociceptive facial receptive fields whose periorbital distribution is similar to the region of referred pain evoked by dural stimulation in humans. In the present study, intracellular labelling with horseradish peroxidase was used to examine the anatomical characteristics of brainstem trigeminal neurons that respond to dural stimulation. A total of 17 neurons was labelled that responded to electrical stimulation of dural sites overlying the superior sagittal sinus or middle meningeal artery. Fourteen of these neurons also responded to electrical stimulation of the cornea. The neurons in this sample were located in the rostral two-thirds of the trigeminal nucleus caudalis and the caudalmost part of the nucleus interpolaris. Within caudalis, the neurons were located in the deeper part of the nucleus, primarily lamina V, and were concentrated ventrolaterally. The dendritic arborizations of the dura-responsive neurons typically exhibited a dorsolateral-to-ventromedial orientation and did not extend into the superficial laminae of caudalis. Dura-responsive neurons had axonal collaterals and boutons in the nucleus caudalis, nucleus interpolaris, the infratrigeminal region ventral to nucleus interpolaris, the nucleus of the solitary tract, and the medullary reticular formation. The axonal boutons within the trigeminal complex exhibited a ventrolateral distribution which largely overlapped the distribution of the somata. The results are consistent with previous evidence that dura-responsive brainstem trigeminal neurons may have a role in the mediation of dural vascular head pain and also indicate that such neurons may contribute to nociceptive processing within the dorsal horn.
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PMID:Anatomical properties of brainstem trigeminal neurons that respond to electrical stimulation of dural blood vessels. 799 55

Poliomyelitis is an acute viral disease that attacks the brain and the ventral horn of the spinal cord. Damage to the lower motor neurons usually results in atrophy and weakness of muscle groups, perhaps paralysis and possibly deformity. A second type, bulbar poliomyelitis, infects the medulla oblongata and may result in dysfunction of the swallowing mechanism along with respiratory and circulatory distress. Minor forms of poliomyelitis result in fever, sore throat, headache, and upper body stiffness, but leave no significant atrophy or paralysis. The purpose of this paper is to review post-polio syndrome (PPS) as well as the effect of exercise on the symptoms and morphologic adaptations to PPS and where future research efforts should be directed. The most common features of PPS for over 350,000 afflicted survivors include general fatigue, weakness, and joint/muscle pain. The primary reasons for these symptoms include 1) destruction of the anterior horn cells by the polio virus, leaving fewer motor neurons to induce muscle contraction; 2) unaffected motor unit enlargement by reinnervation through terminal sprouting; and 3) defective transmission at the neuromuscular junction secondary to failure of terminal axonal sprout. Acute responses to resistive exercise suggest significant muscle strength decrements in the knee extensors compared with similar aged people without polio. However, limited training investigation indicates significant strength increases for the knee extensors following at least 6 wk of training. Acute aerobic responses also differ significantly from those observed in aged-matched control subjects. Chronic aerobic responses to limited training studies suggest significant elevations in maximal oxygen uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Poliomyelitis and the post-polio syndrome: exercise capacities and adaptation--current research, future directions, and widespread applicability. 847

Forty patients who sustained minor head trauma were investigated by brainstem trigeminal and auditory evoked potentials (BTEP, BAEP) and middle-latency auditory evoked potentials (MLAEP). The patients were evaluated within the first 48 h following their admission and at 3 months after the injury. Outcome was scored at the follow-up examination according to six complaints: failure to resume previous professional activity, headache, memory disorders, dizziness and vertigo, behavioural and emotional disturbances, and other symptoms of a neurological nature. Post-concussion syndrome (PCS) was defined by the presence of four or more of the listed features. All three evoked potential modalities showed significantly increased latencies at the initial assessment, disclosing disseminated axonal damage. Unlike the BTEPs and the BAEPs, the MLAEPs proved to correlate to outcome at 3 months, especially in its psychocognitive aspects. These findings suggest that organic diencephalic-paraventricular primary damage may account for the occurrence of PCS.
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PMID:Trigeminal and auditory evoked responses in minor head injuries and post-concussion syndrome. 860 13

Ethylene oxide (EO) is commonly used to sterilize heat-sensitive products used by hospital patients and personnel. Ethylene chlorohydrin (EC), a by-product, is considered highly toxic. We report a cluster of 12 operating-room nurses and technicians who developed symptoms after a 5-month exposure to high levels of EO and EC in disposable surgical gowns. All patients reported a rash on the wrist where contact was made with the gowns, headaches, and hand numbness with weakness. Ten of 12 patients complained of memory loss. Neurologic evaluation revealed neuropathy on examination in nine of the 12 patients, elevated vibration threshold in four of nine, abnormal pressure threshold in 10 of 11, atrophy on head MRI in three of 10, and neuropathy on conduction studies in four of 10. Neuropsychological testing demonstrated mild cognitive impairment in four of six patients. Sural nerve biopsy in the most severely affected patient showed findings of axonal injury. Several patients in this group display signs of peripheral and CNS dysfunction following exposure to EO. Possible mechanisms of neurotoxicity include direct exposure of peripheral nerves through cutaneous absorption and central involvement through inhalation and vascular dissemination. The frequency of central and peripheral nervous system symptoms, supported by objective testing in these EO-exposed patients, suggests other healthcare personnel may be at similar risk.
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PMID:Ethylene oxide neurotoxicity: a cluster of 12 nurses with peripheral and central nervous system toxicity. 878 78

A 38-year-old homosexual male with AIDS suffered four neurological episodes including headaches, confusion, visual impairment, memory disturbances, and dysarthria which resolved spontaneously in a few days. He was admitted to hospital during a fifth episode. Neurological examination revealed a cerebellar syndrome. General examination was normal. CD4 count was 90. CSF contained two WBCs/mm(3) and 12.30 mg/dL protein. MRI revealed diffuse ill defined increased signal on T2-weighted images in the white matter. His condition worsened rapidly with vomiting and he died 1 month after admission. Neuropathological examination revealed diffuse brain oedema with ventricular compression, central diencephalic herniation and bilateral tonsilar herniation in the absence of a focal lesion. Microscopical examination revealed predominant involvement of the white matter with diffuse myelin pallor and massive perivascular dilatation containing an exudate expressing serum proteins and occasional macrophages. The same exudate was also diffuse in the leptomeninges. Parenchymal damage predominated around the perivascular spaces and included loosening of tissue, axonal damage with spheroids and reactive astrocytosis. There was no evidence of productive HIV encephalitis, no multinucleated giant cells; p24 immunostaining and RT-PCR for HIV genome were negative. There was neither significant inflammation nor microglial activation. In this illustrative case, the relapsing course of the neurological signs, the diffuse topography of the blood-brain barrier breakdown and the absence of local cause make it likely that the diffuse leak and axonal damage could be related to circulating factors.
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PMID:Acute, relapsing brain oedema with diffuse blood-brain barrier alteration and axonal damage in the acquired immunodeficiency syndrome. 971 86


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