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

A clinical and neuropsychological syndrome for early recognition of occult hydrocephalus and cerebral atrophy is described. Five illustrative patients are reported. The main features of the syndrome are (i) subjective non-specific complaints (headaches, depression and loss of memory); (ii) the tonic foot response of the sole and the grasp reflex of the foot in the absence of the grasp reflex of the hand; (iii) attacks of sudden and transient loss of muscle tone in both lower limbs leading to falls without warning while standing or while walking. These attacks indistinguishable from drop-attacks are termed chalastic fits; (iv) a dissociation between the satisfactory performances on the Ottawa-Wechsler scale and the poor performances on Kohs Block Design test. Clinical and neuropsychological findings could not differentiate between occult hydrocephalus and cerebral atrophy; only radionuclide cisternography and computerized tomography were able to delineate the final diagnosis.
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PMID:A syndrome of early recognition of occult hydrocephalus and cerebral atrophy. 91 52

Computerized axial tomography of the cranium has been carried out in 46 patients referred because recurring migrainous headaches. Increasing frequency or severity of headaches or a change in headache pattern were the usual reasons for referral. Abnormalities were found in 37 cases and fell into 4 categories. The most frequent (21 cases) consisted of a mild degree of oedema in the white matter of one or both cerebral hemispheres. This was usually bi-frontal (15 patients) but was more extensive in 2 patients. Varying degrees of cerebral atrophy, as determined by widening of the Sylvian, brain-stem and interhemispheric cisterns, and/or widening of the third and lateral ventricles as compared to a group of normal scans, was found in 8 cases. Areas of occipital infarction were found in 4 patients with permanent visual field defects. Unexpected small areas of infarction were found in the temporal lobe in 2 other cases. Cerebral tumours were found in 2 cases. The significance of these findings is discussed, as well as the possible role of migrainous vaso-spasm with consequent changes in cerebral blood flow in the pathogenesis of oedema and atrophy in migraine subjects.
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PMID:Computerized axial tomography findings in a group of patients with migrainous headaches. 102 5

Thirty-eight workers from a factory producing nickel-cadmium and other types of batteries came to us for medical evaluation. They included 21 women and 17 men (seniority 2-20 years, age range 31-63 years), and represented a self-selected subset of 700-900 ever-employed and 200+ recently or currently employed workers in the factory. Thirty-four worked on the nickel-cadmium assembly line. Symptoms and signs included: headache in 34; weakness, fatigue and lassitude in 26; dizziness in 16; pruritus and skin eruptions in 37; gingivitis, teeth loss and caries in 34; nasal congestion, nosebleeds and anosmia in 30; cough, phlegm production, wheezing and shortness of breath in 26; "asthma" in 14; bone pain in 18; urinary frequency, beta 2 microglobulinuria and kidney stones in 17; and sterility or multiple abortions (33) in 8 of 21 women. One additional patient had died from an "amyotrophic lateral sclerosis-like syndrome", while CT scans in six workers revealed brain atrophy. One other worker had leukemia, and two had died from cancer (lung and pancreas). Those who had worked for more than 10 years had more symptoms and signs than shorter-term employees, especially neurological illness, bone pain and urinary tract problems, including beta 2 microglobulinuria. Past blood and urinary cadmium levels were in the range of 1.6-8.7 micrograms/dl and 8-306 micrograms/l, respectively. Our findings indicated that: a) health risks for workers were not confined to the nickel-cadmium assembly line or to older workers, b) hazardous exposures still existed and illness appeared in new workers after a clean-up and intervention program, and c) exposures involved increased risks for renal disease and cancers. Finally, there is a need to control exposures and determine health risks in the full cohort of those ever employed, in the workers' children, and in the surrounding environment (air, ground, water) due to the dumping of waste from the plant.
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PMID:Medical findings in nickel-cadmium battery workers. 142 13

Head injuries have been shown to account for between 4 and 22% of soccer injuries. Clinical and neuropsychological investigations of patients with minor head trauma have revealed organic brain damage. 69 active football (soccer) players and 37 former players of the Norwegian national team were included in a neurological and electroencephalographic (EEG) study to investigate the incidence of head injuries mainly caused by heading the ball. 3% of the active and 30% of the former players complained of permanent problems such as headache, dizziness, irritability, impaired memory and neck pain. 35% of the active and 32% of former players had from slightly abnormal to abnormal EEG compared with 13 and 11% of matched controls, respectively. There were fewer definitely abnormal EEG changes among typical 'headers' (10%) than among 'nonheaders' (27%). The former players were also subjected to cerebral computed tomography (CT), a neuropsychological examination and a radiological examination of the cervical spine. One-third of the players were found to have central cerebral atrophy and 81% to have from mild to severe (mostly mild to moderate) neuropsychological impairment. The radiological examination of the cervical spine revealed a significantly higher incidence and degree of degenerative changes than in a matched control group.
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PMID:Head and neck injuries in soccer. Impact of minor trauma. 143 95

Patients investigated at our institute during the last decade included 166 (1.2%) who showed uni- or bilateral basal ganglia calcification on computed tomography. We tested the significance of this neuroradiological observation by statistical comparison of these patients' clinical disorders with the findings in a random sample of 622 patients without basal ganglia calcification. The odds for the most common neurological disturbances were similar in patients with and without basal ganglia calcification. After adjustment for differences in age and brain atrophy there was no evidence of a significantly increased risk of dementia (odds ratio 1.1), cerebral infarction (1.4), epilepsy (0.9), vertigo (1.6), headache (1.8), or alcoholism (0.9), which represented the most common diagnoses. We conclude that basal ganglia calcification cannot be considered as a clinically relevant neuroradiological finding in the majority of cases and that it should not be used as an explanation for frequently observed neurological disturbances.
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PMID:Neurological disorders in 166 patients with basal ganglia calcification: a statistical evaluation. 154 67

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

69 active football (soccer) players and 37 former members of the Norwegian national team were included in a neurological and electroencephalographic (EEG) study to investigate the incidence of head injuries, mainly caused by heading the ball. 3% of the active players and 30% of the former players complained of permanent problems such as headache, dizziness, irritability, impaired memory and pain in the neck. 35% of the active players and 32% of former players had from slightly abnormal to abnormal EEG, as against 13 and 11% of respective matched controls. There were fewer definitely abnormal EEG changes among typical headers (10%) than among "non-headers" (27%). The former players were also subjected to cerebral computed tomography (CT), a neuropsychological examination and a radiological examination of the cervical spine. One third of the players were found to have central cerebral atrophy and 81% to have from mild to severe (mostly mild to moderate) neuropsychological impairment. The radiological examination of the cervical spine revealed a significantly higher incidence and degree of degenerative changes than in a matched control group.
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PMID:[Head and neck injuries among Norwegian soccer players. A neurological, electroencephalographic, radiologic and neuropsychological evaluation]. 157 6

The present report documents a family with three cases in two successive generations of pigmentary orthochromatic leukodystrophy (POLD). The clinical features of these cases and histochemical and ultrastructural investigations of two of the brains from successive generations are discussed. A review of the familial cases of POLD reported in the literature is also presented. Transmission of these cases was by a dominant inheritance. Onset of the clinical symptoms occurred at 42 to 54 years of age; duration of the disease was from 2-11 years, and death occurred at 45 to 57 years of age. Clinical manifestations of all three cases were severe headaches; bilateral pyramidal, pseudobulbar, cerebellar, and frontal release signs; gait disturbances; euphoria, or apathy; epileptic seizures; and dementia. The neuropathological pattern consists of slight cerebral atrophy, brownish discoloration of the cerebral white matter with demyelination and severe gliosis, sparing the sub-cortical U fibers; presence in the macrophages of lipid pigment granules that are sudanophilic, non metachromatic, and PAS and iron positive. The electron microscopic pattern of the lipid pigment in the macrophages is that of ceroid: electron-dense, membrane-bound intracytoplasmic lysosomes with curvilinear and/or fingerprint profiles.
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PMID:The dominant form of the pigmentary orthochromatic leukodystrophy. 172 27

Cerebral magnetic resonance imaging (MRI) was performed on 18 patients with migraine characterized by aura consisting of both visual symptoms and paresthesias. Fifteen headache-free individuals of the same age range were used as controls. Records were randomized and read in blind fashion by two neuroradiologists. Small subcortical white matter lesions were seen in three migraine cases and two controls. In one migraine case cortical infarctions were seen. In two controls, small areas of increased density similar to those in migraine were seen. No consistent correlation of migraine or its duration with cerebral atrophy was found. It is concluded that identification of both these MRI findings (small subcortical white lesions and cerebral atrophy) as significantly associated with migraine is doubtful.
Cephalalgia 1991 Jul
PMID:Magnetic resonance image abnormality in migraine with aura. 188 71

We compared cranial CTs of 35 habitual cocaine abusers, 16 self-reported 1st-time users, and 54 headache patients using linear planimetric measures. All patients met the following criteria: age 20 to 40 years, no polydrug abuse (including alcohol), HIV seronegativity, normal albumin level, and no history of any other neurologic disease. The sex ratios and ages were not significantly different in the 3 groups. The planimetric measurements and calculated indices of cerebral atrophy were significantly different in the habitual cocaine abusers compared with the 2 other groups of patients. There were no differences between 1st-time cocaine users and controls. Among the habitual cocaine abusers there was a positive correlation between the approximate duration of cocaine abuse and the calculated atrophy indices. The findings suggest that cerebral atrophy develops in chronic cocaine abusers, and the severity correlates with the duration of abuse.
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PMID:Cerebral atrophy in habitual cocaine abusers: a planimetric CT study. 174 38


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