Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 75-year-old woman with a dural arteriovenous fistula (DAVF) presented with progressive cognitive impairment including amnesia and alexia. Neuroradiological studies showed a relatively confined DAVF lesion in the left temporal lobe. The patient did not have a history of trauma and did not complain of headache or tinnitus. Amnesia and alexia dramatically improved upon treatment of the DAVF, and this was associated with attenuation of an abnormal MRI signal in the left temporal lobe. The results suggest that gradually impaired cerebral circulation due to focal venous hypertensive encephalopathy localized to the left temporal lobe and resulting from a DAVF could be involved in slowly progressive amnesia and alexia. The case also shows that an intracranial DAVF may present as a variety of neurological symptoms, depending on its localization, size and clinical stage.
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PMID:Focal dural arteriovenous fistula (DAVF) presenting with progressive cognitive impairment including amnesia and alexia. 1770 15

65 patients with a mild craniocereberal trauma have been observed. Medical examination included among general clinical methods the following methods: KT (MRT) of the brain, oculist examination including the observation of eye fundus. For objectification of a patient' complaints the authors used orientation and Galvestona's amnesia tests, feeling scale (psychological test), the table to determine the level of memory. Tests have been carried out on the first, tenth and thirty day of the treatment. Patients of the first group received in a complex treatment -pramistar, patients of the second group - piracetam. Patients of both groups noted considerable improvement during a complex treatment (disappearance of headache, dizziness and nausea) and at the same time patients receiving pramistar had better restoration of orientation and feeling. Pramistar was also more effective in patients with amnesia.
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PMID:[Application of nootropic agents in complex treatment of patients with concussion of the brain]. 1841 26

This was a prospective, observational study of children aged 3 to 15 years admitted to hospital with head injury (HI). Demographic data and information on the nature of the HI, and history of premorbid headache were collected. A structured telephone questionnaire was used to interview parents and children 2 months after injury and at 4-monthly intervals for up to 3 years, if headache was reported. One hundred and ninety children were admitted with HI. Data were available on 117 children (81 males, 36 females; mean age 8y 5mo [SD 3y 1mo]). HI was minor in 93 patients and significant in the rest. Minor HI was defined as a closed injury, no loss of consciousness, and a Glasgow Coma Score (GCS) of 13 to 15. Significant HI was associated with loss of consciousness for >30 minutes, GCS of <13, and post-traumatic amnesia for >48 hours. Eight children (five males, three females; mean age 10y 7mo [SD 2y]) reported chronic post-traumatic headache (CPTH). Five children had episodic tension-type headache and three had migraine with or without aura. Headache resolved over 3 to 27 months in all except one child who was lost to follow-up. Premorbid headache in three children transformed in frequency and type following HI. These patients were excluded from the study. CPTH is common after minor and significant HI. It has the clinical features of tension-type headache and migraine and has a good prognosis.
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PMID:Chronic post-traumatic headache after head injury in children and adolescents. 1842 78

In this study, a total of 17 adult patients ((> or =18 years old; 12 male, 5 female) with encephalitis followed up in neurology and infectious diseases clinics of Trace University Hospital between the years 2000-2005 were retrospectively analyzed. The most common signs and symptoms were confusion (n: 13; 76.4%), nausea and vomiting (n: 13; 76.4%), disorientation (n: 12; 70%), fever and headache (n: 11; 64.7%), amnesia (n: 10; 58.8%), convulsions (n: 9; 52.9%), agitation (n: 7; 41%), dysphasia and aphasia (n: 6; 35.2%), nuchal stiffness (n: 5; 29.4) and focal neurological signs (n: 1; 5.8%). Six of the patients were admitted to the hospital during summer, six during winter, four during spring and one during autumn. Eleven (64.7%) of the patients had electroencephalographic signs compatible with encephalitis. Encephalitis related signs were detected in 83.3% (10/12) of the patients by cranial magnetic resonance imaging and in 58.3% (7/12) by computerized tomography. Cerebrospinal fluid (CSF) examination revealed low glucose levels in 17.6% (3/17), high protein levels in 47% (8/17) and increased white blood cells with a predominance of lymphocytes in 41.2% (7/17) of the cases. CSF findings were within normal limits in 23.5% (4/17) of the patients. Empirical acyclovir treatment was given to all patients. One patient died at the acute phase of the infection while all the other 16 recovered. Since none of the CSF samples yielded bacterial growth, all of the patients were diagnosed as viral encephalitis. However, no investigation was performed to identify the viral etiology and this was the major limitation owing to the inadequacy of laboratory facilities during the study period and/or unawareness of the physicians about viral identification methods.
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PMID:[Retrospective evaluation of the cases prediagnosed as viral encephalitis in Trace University Hospital between the period of 2000-2005]. 1869 29

A 34-year-old man was admitted with his unsteady gait, difficulty in speech and a paroxysmal severe headache accompanied with sensori-motor disturbance of the right extremities and aphasic symptom. His family history was unremarkable. His unsteadiness has progressed very slowly from childhood. He noted to be inarticulate at the age of 18 years. At the age of 33 years, he suddenly had an attack of severe throbbing headache, which was mainly left parietal, with nausea and photophobia. During the headache, his right extremities were paralyzed and he became aphasic. He had lost a partial memory of the event All these symptoms had gone within 24 hours. Thereafter, the same headache occurred about once a month. Neurological examination revealed a mild truncal ataxia and ataxic dysarthria. Electroencephalography (EEG) showed intermittent delta waves restricted over the left fronto-temporal region. Brain MRI showed a moderate atrophy of superior cerebellar vermis and anterior cerebellar lobe. The diagnosis of sporadic hemiplegic migraine (SHM) with cerebellar ataxia was made. Our case was very similar to familial hemiplegic migraine (FHM) 1, of which some families are accompanied with transient amnesia, cerebellar ataxia and EEG abnormality. Although we did not detect any mutations in CACNA1A gene previously reported in FHM1, our case might share same pathogenesis with FHM1.
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PMID:[Case of sporadic hemiplegic migraine with cerebellar ataxia]. 1959 4

We report the clinical findings and neuropsychological profiles of a sample of patients exhibiting a focal retrograde amnesia (FRA) seen consecutively during the period 1992-2007. The cohort comprised 13 patients, five males, with a mean age of 30 years (range 16-49). They were given a neurologic examination, psychiatric interview and formal neuropsychological examination (all but one) during the amnesic phase, underwent neuroimaging, and were followed up for six months to ten years. All presented with an acute amnesia characterized by an impaired recollection of memories predating the acute event, with spared or minimally and transiently affected anterograde memory, thus consistent with FRA. The events triggering FRA varied widely: mild to severe head injury, road accident without head injury, seizure, dissociative fugue, BDZ overdose, posttraumatic headache, syncope, migraine attack, acute distress. The neuropsychological hallmark of FRA was a selective or prominent impairment of autobiographical memory. The defect was often so severe as to cover most or all of the patients' lives and, in some cases, to erase the knowledge of their own identity. Conventional neuroimaging (brain CT and MRI) was unimpressive. Cerebral SPECT/PET disclosed unilateral frontal hypoperfusion in three (two left). All but one patient fully recovered, time of recovery ranging from three days to six months. FRA is a condition reflecting a block of memory function triggered by heterogeneous events, including both physical and psychic insults. Analogies shared with the more frequently encountered and better known condition of transient global amnesia suggests common pathogenetic mechanisms. A tentative nosographic classification of FRA is finally offered.
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PMID:When the past is lost: focal retrograde amnesia. Focus on the "functional" form. 1964 Dec 49

Topiramate is a highly effective drug in migraine prophylaxis and is considered a first-line treatment. The evidence for the efficacy of topiramate is based upon the results of several large, randomized, double-blind, placebo-controlled trials. Adverse events (AEs) are common and require discontinuation of the treatment in about 20-25% of patients, but they are rarely severe. There are reviews regarding topiramate-related AEs representing a large number of patients treated in controlled trials. The most common AEs are weight loss, dizziness, somnolence, abnormal thinking, fatigue, ataxia, confusion, paresthesias, impaired concentration, nervousness, amnesia, and language difficulties. The development of cough has never been reported as an AE during topiramate prophylaxis for migraine. We present 3 cases in which the prophylactic treatment for migraine with topiramate was discontinued due to the onset of primary intractable coughing.
Headache 2010 Feb
PMID:Topiramate-induced intractable cough during migraine prophylaxis. 1975 66

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43

Antiphospholipid syndrome (APS) is an autoimmune disease with recurrent thromboses and pregnancy complications (90% are female patients) that can be primary and secondary (with concomitant autoimmune disease). Antiphospholipid antibodies are prothrombotic but also act directly with brain tissue. One clinical and one laboratory criterion is necessary for the diagnosis of APS. Positive serological tests have to be confirmed after at least 12 weeks. Clinical picture consists of thromboses in many organs and spontaneous miscarriages, sometimes thrombocytopaenia and haemolytic anaemia, but neurological cases are the most frequent: headaches, stroke, encephalopathy, seizures, visual disturbances, Sneddon syndrome, dementia, vertigo, chorea, balism, transitory global amnesia, psychosis, transversal myelopathy and Guillain-Barre syndrome. About 50% of strokes below 50 years of age are caused by APS. The first line of therapy in stroke is anticoagulation: intravenous heparin or low-weight heparins. In chronic treatment, oral anticoagulation and antiplatelet therapy are used, warfarin and aspirin, mostly for life. In resistant cases, corticosteroids, intravenous immunoglobulins and plasmapheresis are necessary. Prognosis is good in most patients but some are treatment-resistant with recurrent thrombotic events and eventually death.
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PMID:[Antiphospholipid syndrome in neurology]. 2118 99

Insulinoma, usually benign (90%), is clinically characterized by symptoms as tremulousness, tachycardia, weakness, sweating, fatigue, hunger, headache, dizziness, disorientation and unconsciousness. However rarely it has an unusual presentation. We present a case of insulinoma misdiagnosed as neurologic disease. A 48-year-old man was admitted to our Emergency Division because of car accident caused by loss of consciousness. A diagnosis of complex partial seizure was made one year before. The patient appeared pale, tachycardic, BP 130/85 mmHg. Laboratory tests showed a severe hypoglycemia (30 mg/dl). He was treated with hypertonic glucose solution and the resolution of symptoms was obtained. Dosages of insulin and C-peptide, CT-scan and RMN confirmed a diagnosis of insulinoma. Seizure disappeared after surgical excision. The diagnosis of insulinoma is sometimes delayed up to more than 20 years. Neurologic or psychiatric presentation like disorientation, personality changes, amnesia, irritability, seizures, bizarre behavior, visual difficulties, neuropathy in patients affected by insulinoma could be cause of misdiagnosis. Diagnosis of insulinoma should always be considered whenever these symptoms occur, especially if unresponsive to specific therapy. Insulinoma is curable in most cases and an early diagnosis can avoid adverse consequences including neurologic damage.
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PMID:[Complex partial seizure in patient with insulinoma: importance of early diagnosis]. 2135 8


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