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

Previous studies have shown that migraine with aura is associated with the reduction of regional cerebral blood flow (rCBF). However, the question of whether the reduction of rCBF during migraine aura is caused by cerebral vasospasm or is secondary to the neural depression (spreading depression) is still disputed. We measured rCBF by high resolution SPECT method during the attack of migraine and examined whether the reduction in flow corresponds to the cerebral vascular territory. Fourteen patients with migraine with aura (7 men and 7 women, 34.7 +/- 17.8 years) were studied. In all the patients rCBF was measured during the interictal period and in four patients rCBF was measured during the aura of migraine. SPECT measurements of rCBF was performed using Tc-99m-PAO (740 MBq) as a tracer. During the aura of scintillation scotoma in the unilateral visual field rCBF was reduced in the opposite occipital, temporal and thalamic regions which corresponded clearly to the region of the posterior cerebral arterial territory. The reduction of rCBF was by 31 approximately 49% compared with the opposite hemisphere. Cerebral spinal fluid lactate level during the headache measured in one patient was higher (38 mg/dl) than the interictal period (12 mg/dl). Our data indicated that the reduction of rCBF during the aura is caused by ischemia probably due to the cerebral vasospasm and is not secondary to the neuronal depression. It was also suggested that the primary site of rCBF reduction during the visual aura is the occipital association cortex which is reported to be responsible for the visual hallucination.
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PMID:[Regional cerebral blood flow during migraine]. 875 89

Visual hallucinations are commonly associated with seizures, drug effects, psychiatric disorders, or visual loss as 'release' phenomena. We report the case of a previously healthy 65-year-old woman, who was admitted to hospital with intermittent headache episodes accompanied by complex visual hallucinations. During these episodes the patient's blood pressure was 220/120 mmHg. In between symptomatic episodes she had no complaints and felt healthy. The neurological and ophthalmological examinations were normal but cerebral magnetic resonance imaging (MRI) showed multiple white matter abnormalities in the parieto-occipital regions. Rapid reversal of the symptoms and imaging abnormalities occurred concurrently with lowering of blood pressure. The history and the findings were similar to those recently described in the clinicoradiological 'posterior leukoencephalopathy' syndrome. Different pathogenic mechanisms are discussed. Copyright 1998 Lippincott Williams & Wilkins
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PMID:Visual hallucinations in a case of reversible hypertension-induced brain oedema. 1021 Aug 99

Neurocysticercosis is common in Asia, Africa and South America including Mexico. A diagnosis of neurocysticercosis was made neuroradiologically in an 8-year-old Mexican girl, who had suffered from learning difficulties for a year, and subsequently developed headache, vomiting, gait disturbance, visual hallucination, apraxia and euphoric state for 4 months. Plain CT demonstrated numerous cystic lesions with or without scolex in addition to calcified lesions. The lesions were seen throughout the whole brain, although they were relatively scarce in the cerebellum and the lateral ventricular system. Although edema was prominent around the bilateral ventricles, neither ventricular dilatation, midline shift nor inflammatory reaction around the cysts was detected. The patient was treated with albendazole for a month and with steroid for two months. Headache and vomiting disappeared in the first week of treatment but other symptoms persisted, with fluctuation. CT after 2 months of treatment showed dilatations of the third and lateral ventricles. Despite massive infection in the brain, the clinical picture at onset was mild and compatible with nonencephalitic cerebral cysticercosis. The symptoms might be caused by the progressive hydrocephalus due to cerebrospinal fluid blockage, the prognosis of which is predicted to be poor.
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PMID:[A Mexican case of massive nonencephalitic neurocysticercosis]. 1602 97

Neurologic signs and symptoms are common in acute malarial infection. However, after the parasites have been cleared from the blood and patients recover full consciousness, neurologic or psychiatric symptoms may occur or recur within 2 months after the acute illness. This phenomenon is called "postmalaria neurologic syndrome" (PMNS). We present a 50-year-old man who returned from the Republic of Malawi and soon developed Plasmodium falciparum malaria. Cerebral malaria, renal failure, hepatic failure, diffuse intravascular coagulation with thrombocytopenia, and upper gastrointestinal bleeding were noted during the acute stage. He was admitted to the infectious diseases ward and treated for 3 weeks. He was free from clinical general symptoms and parasites in blood smear when discharged. However, 2 weeks after discharge, he began to experience severe headache, dizziness, diplopia, mild hand tremor, unsteady gait, and easy falling. When readmitted to the neurologic ward, he presented with irritability, delirium, visual hallucination, and strange behavior. Neurologic examination was normal except for mild general weakness and evident truncal ataxia when walking. Brain magnetic resonance imaging revealed no structural lesions, and electroencephalography showed diffuse cortical dysfunction. Cerebral spinal fluid profile exhibited cytoalbuminologic dissociation. Brain single photon emission computed tomography showed diffuse cerebral parenchymal disorder. Nerve conduction studies revealed early sensory predominant polyneuropathy. The unsteadiness persisted for the initial 2 weeks of hospitalization until corticosteroid was administered. Intravenous methylprednisolone (80 mg/day) was continued for 3 days, followed by oral prednisolone (45 mg/day). His unsteadiness improved gradually after medication, and he absconded from the hospital on the 9th day of corticosteroid treatment with clear consciousness and free ambulation. The manifestation of PMNS is diverse and may present as an acute confusional state or psychosis, generalized seizure, fine tremors, cerebellar syndromes, postural hypotension, or malarial polyneuritis. Although the neurologic syndrome is primarily self-limited in most cases, corticosteroid may be beneficial in reversing PMNS.
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PMID:Postmalaria neurologic syndrome: a case report. 1711 25

Charles-Bonnet syndrome (CBS) occurs after the loss of vision or a decrease in visual ability and is characterized by visual hallucinations with insight and preserved cognitive status. In this paper, 2 cases in which vision was lost (in one patient due to hypophyseal macroadenoma and in the other due to diabetic retinopathy) are presented. The first case is a 35-year-old male referred to the psychiatry department for depressive complaints. He lost his vision due to optic atrophy following multiple surgeries for hypophyseal macroadenoma and visual hallucinations developed afterwards. Ziprasidone 80 mg/day was started and the hallucinations disappeared on the fifth day, but the medication had to be withdrawn because of severe vascular type headaches. Olanzapine 5 mg/day was subsequently used without benefit. He refused further medication and the visions gradually changed into sparkling lights and simple figures at the 7-month follow-up. The second case was a 54-year-old woman with a 20-year history of type-II diabetes mellitus. Visual hallucinations developed after bilateral visual loss due to diabetic retinopathy 4 years earlier. She responded well to treatment with quetiapine 100 mg/day and paroxetine 20 mg/day. Neither of the cases had reported their visual symptoms to their physicians; the second case was diagnosed after 4 years by active screening. Both of the cases had neuroanatomic lesions. CBS symptoms should be screened actively in patients with visual loss and physicians should be educated about diagnosing CBS. Novel antipsychotics, such as ziprasidone and quetiapine, seem to be effective alternatives for the treatment of CBS.
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PMID:[Charles-Bonnet Syndrome: a report of two cases]. 1785 83

A case of visual hallucination, headache and left hemiparesis is reported. The patient had a history of recurrent attacks of similar semiology for the previous 15 years. MRI brain revealed a cortical hyperintensity on T2W, FLAIR and diffusion weighted imaging (DWI) in the right cerebral hemisphere with a normal ADC (apparent diffusion coefficient) map and MR angiogram. Detailed workup for MELAS was negative. A diagnosis of sporadic hemiplegic migraine was made and he was managed conservatively. He made a gradual complete recovery over 2 weeks. He was discharged on flunarizine for prophylaxis and has remained asymptomatic over the ensuing 4 months. This interesting condition is reviewed and discussed herein.
J Headache Pain 2008 Dec
PMID:Sporadic hemiplegic migraine: report of a case with clinical and radiological features. 1881 Mar 16