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

Iatrogenic pathology of the optic nerve is examined according to a framework which distinguishes direct and indirect effects on the optic nerve. Direct effects due to toxic drugs should be suspected when unexplained, usually bilateral loss of visual acuity occurs. The 3 clinical stages of classical optic toxic neuropathy are 1) anomalies of color vision, 2) loss of visual acuity and narrowing field of vision, and 3) papillary palor corresponding to irreversible optic atrophy. Usually only the 1st stages are reversible, but the reversibility may be incomplete. The list of drugs which can cause such effects is lengthy and includes antiinfectious drugs such as sulfamides and derivatives of hydroxyquinoleins, chloramphenicol especially when used to treat cystic fibrosis of the pancreas in children, the antituberculins ethambutol in high doses and isoniazide, which occasion particular risks when combined; antiparasitics such as quinine and its derivatives chloroquine and hydroxychloroquine, which cause optic neuropathy through their effect on the retina; arsenic pentavalents such as tryparsamide, quinacrine, trecator and mystatin; drugs affecting the central nervous system such as monoamineoxydase inhibitors, laroxyl, phenothiazine and the barbituates; anticonvulsants such as phenytoin; antimitotics such as vincristine; digitalics, disulfiram; penicillamines, and pexid. The action of lasers on the optic nerve can have a similar effect. The optic nerve may be indirectly damaged during surgical procedures leading to hypotonia, acute ischemia of the head of the optic nerve or embolic accident after a local or regional injection. Damage may also be caused by radiotherapy of intracranial tumors and certain drugs which cause isolated papillary edema or edema associated with headaches, such as Tetracycline, large doses of vitamin A or D, corticoids, and oral contraceptive (OC) pills, which may cause papillary edema through cerebral pseudo-tumors that regress with discontinuation of treatment. This condition has been observed in women with uncontrolled hyperlipidemia. It is probable that an alteration ofaxonal transport is at the basis of the neuropathic mechanisms. The 1st step in therapy is the suppression of the toxin, or at least its discontinuation. Some success has been obtained with vitamin B therapy, corticotherapy, zinc, or isaxonine, depending on the specific condition.
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PMID:[Iatrogenic pathology of the optic nerve]. 676 92

A familial optic atrophy with X-recessive heredity, distinct from Leber's optic atrophy (LOA), is described. The symptoms are: slight to moderate pallor of the papillomacular bundle at the disc possibly preceded by some hyperaemia of the disc, telangiectasia on the disc with normal retinal vessels, occurrence in the second decade of life, slow progression with often subclinical visual loss, a small relative central scotoma with an intact peripheral visual field, slight acquired tritanopia and deuteranopia, and vasomotor headaches. The disease may exhibit severe exacerbations with loss of vision to 1/60, provoked by vasoconstrictors and reacting favourably to vasodilators. This acute loss of vision is associated with ischaemia of the disc, a deep central scotoma with marked disturbance of colour vision in the form of an acquired deuteranopia, and sensoparalytic pupils. This is followed by increasing pallor of the disc, slow resolution of the central scotoma with a permanent reduction in the central light sensitivity, markedly disturbed Visual Evoked Potentials (VEP), acquired deuteranopia and normal ERG and EOG. In contrast to all hereditary opticopathies so far described, fluorescein angiography showed a disturbance of perfusion in the peripapillary choroid and the prelaminar part of the optic nerve. A similar disturbance of perfusion is described in anterior ischaemic optic neuropathy (AION) and low-tension glaucoma. To these acquired, non-hereditary recessive vascular opticopathies, which usually occur late in life, will have to be added the X-recessive vascular optic atrophy which we describe here, for which we propose the name: X-recessive angiopathic opticopathy. The differential diagnosis from some other hereditary, especially X-recessive, optic atrophies is discussed.
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PMID:X-recessive angiopathic opticopathy. 706 94

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 Limousin region had at present one of the largest elderly populations in France and in Europe. To determine the frequency of certain neurological disorders in the elderly, a neuroepidemiological survey was conducted in 1986-1987 on a representative sample of the population in Haute-Vienne (the most population-dense department in the Limousin region). This study used a WHO protocol which was first introduced at the beginning of the 1980s. It had been previously tested in France on a pilot population in 1984. The prevalences of the principal neurological disorders encountered per 100,000 inhabitants were as follows: nonmigraine headache 5,059, migraine 4,270, epilepsy 788, completed stroke 1,445, transient ischemic attacks 657, neuropathy 1,642, Parkinson's disease 328, and dementia 197.
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PMID:Prevalence of neurological disorders in Haute-Vienne department (Limousin region-France). 764 54

Two young males from Central Province were referred to Port Moresby General Hospital with chronic headaches. In each case the initial impression of tuberculous meningitis needed revision in the light of strongly positive cryptococcal serology. Cryptococcal meningitis occurs with sufficient frequency in Papua New Guinea that it should be considered in cases of raised intracranial pressure, ataxia, cranial neuropathy and visual disturbances. Delay in treatment may be disastrous. In contrast to the developed world where fungal meningitides show a predilection for the immunosuppressed, the experience to date in Papua New Guinea is that the majority of cases in both adults and children occur in ostensibly immunocompetent individuals. The epidemiology, clinical course and current treatment of this potentially curable disease are discussed.
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PMID:Cryptococcal meningitis in children in Papua New Guinea: a reminder. 766 53

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

Three HIV-infected patients developed cranial neuropathy as the initial manifestation of an AIDS-related large cell lymphoma. All were homosexual men known to be HIV seropositive for 3 to 4.5 years. At the time of presentation for neurological disease, the CD4 T-lymphocyte count was < 400 cells/mm3 in each. Initial manifestations were retro-orbital headache and oculomotor nerve palsy in two and an abducens nerve palsy in the other. Repeatedly negative CSF cytologies and recovery of the cranial neuropathy obscured the diagnosis. These patients illustrate that cranial neuropathy with HIV infection may herald the presence of an occult large cell lymphoma. Spontaneous or corticosteroid-associated improvement of the cranial neuropathy, absence of abnormalities on brain imaging studies, and negative CSF cytologies do not exclude this diagnosis. We suggest that a diligent and repeated search for lymphoma be considered in HIV-infected patients presenting with cranial neuropathy, including repeated CSF examinations, MRI of brain and spine (T1 and T2) with and without gadolinium enhancement, chest and abdominal CT scans, and bone marrow biopsy.
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PMID:Cranial neuropathy heralding otherwise occult AIDS-related large cell lymphoma. 810 48

We report three patients with chronic headaches and optic neuropathy due to widespread meningeal thickening shown on enhanced MRI; all had biopsy-proven intracranial pachymeningitis (fibrosclerosis of the meninges). Two patients had bilateral optic neuropathy, elevated CSF protein, and polyclonal serum hypergammaglobulinemia. They developed temporal lobe cortical necrosis or sagittal sinus thrombosis, presumably due to compromised dural venous drainage from extensive meningeal fibrosis. The other patient had multiple cranial nerve palsies and unilateral optic neuropathy with normal CSF. Corticosteroid therapy improved visual function in all three patients, although all had persisting visual deficits. Gadolinium-enhanced MRI was essential in identifying meningeal inflammation and locating suitable biopsy sites.
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PMID:Visual loss from idiopathic intracranial pachymeningitis. 816 28

Eosinophilic meningitis or meningoencephalitis is a disease commonly seen in Taiwan, especially in children during the summer rainy season. Most of the cases reported in other countries were adults and their clinical manifestations were different from children. Studies on special clinical characteristics among 87 children in Taiwan were performed. Thirty-eight (43.7%) were male and 49 (56.3%) females, and 88.5% could be traced to a history of contact with the intermediate host, the giant African snail, Achatina fulica, which plays a major role in transmission. The incubation period (average: 13.0 days) was shorter in children than in adults (average: 16.5 days). Near thirty percent (28.7%) of the total cases, the clinical form was meningoencephalitis, which was higher than in adult cases seen in Thailand (5%). The most common clinical symptom was fever (92.0%), followed by vomiting and headache. The percentages of sixth and seventh cranial neuropathy associated with the disease were 17.2% and 11.5% respectively. Ophthalmologic fundoscopy showed that 23.0% with papilledema which was significantly higher than seen in adults (12%) in Thailand. Most of the cases in this study had peripheral leukocytosis (above 10,000/mm3) and eosinophilia (above 10%); the percentages were 83.9% and 85.1%, respectively. The worm recovery rate from cerebrospinal fluid by lumbar puncture of 87 cases was 43.7%; 141 worms were collected from one female patient using a pumping method. In the recent 3 years, levamisole was used clinically with good result.
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PMID:[Eosinophilic meningitis and meningoencephalitis in children]. 818 88

To delineate the spectrum of neurologic manifestations and the relative frequencies of different syndromes associated with North American Lyme disease, we describe 96 children referred for neurologic problems in the setting of Borrelia burgdorferi infection. The most frequent neurologic symptom was headache, and the most common sign was facial palsy. Less common manifestations were sleep disturbance, and papilledema associated with increased intracranial pressure. Signs and symptoms of peripheral nervous system involvement were infrequent. The most common clinical syndromes were mild encephalopathy, lymphocytic meningitis, and cranial neuropathy (facial nerve palsy). In contrast with adult patients with neurologic Lyme disease, meningoradiculitis (Bannwarth's syndrome) and peripheral neuropathy syndromes were rare. However, a "pseudotumor cerebri-like" syndrome seems to be unique to North American pediatric Lyme disease.
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PMID:Neurologic manifestations in children with North American Lyme disease. 825 65


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