Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptoms of migraine can be very atypical during childhood and adolescence. This article describes a case in which the symptoms of migraine were mainly psychiatric: dreamy state, intermittent confusion, partial amnesia, and childlike regressive behavior with depressive features. Although the results from neurological examinations and electroencephalographic recordings were normal when the individual was symptomatic or not, temporal lobe dysfunction, determined by 99mTc-hexamethyl-propyleneamine oxamine single-photon emission computed tomography, was evident during the migraine.
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PMID:Case study: dreamy state and temporal lobe dysfunction in a migrainous adolescent. 789 69

We report two children with acute confusional migraine (ACM) and another with migrainous infarction (MI), aged 7-12 years. There was a family history of migraine in all patients. The patients, who were all right-handed, all manifested sudden onset of consciousness disturbance and other neurological deficits as the first aura in their life. The symptoms in all cases almost completely resolved spontaneously within 24 h, but transient occipital slowing on EEG with laterality corresponding to the side of migrainous origin lasted more than 24 h. In the cases of ACM in the critical phase, although MRI and MR angiography showed no abnormal findings, IMP-SPECT performed within 48 h of migraine attacks revealed a regional change in cerebral blood flow, which is one particular case demonstrated hypoperfusion in the left posterior cerebral artery (PCA) territory. Therefore, although ACM was diagnosed clinically by exclusion, SPECT was thought helpful for the diagnosis of ACM. We speculated that transient hypoperfusion affecting the dominant-sided PCA territory involving the medial temporal structures was responsible for the confusion with amnesia in ACM, in contrast to the lack of confusion or amnesia in the case of MI showing cystic encephalomalacia in the right thalamic and hippocampal regions.
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PMID:Acute confusional migraine and migrainous infarction in childhood. 910 64

We report a case of migraine-associated ischemic stroke causing amnesia, wherein treatment with propranolol may have been contributory. The possible mechanisms involved in migrainous stroke occurring in association with use of propranolol are discussed.
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PMID:Migrainous stroke causing thalamic infarction and amnesia during treatment with propranolol. 938 61

We report the case of a 42-year-old man with repeated attacks of headache associated with retrograde amnesia. Neuropsychological tests before and after the major episode of amnesia showed mild neuropsychological deficits but with spared anterograde memory and learning functions. The amnesia was dense for a period of 15-20 years and included people and events (public and private). There was also a suggestion of amnesia for learned skills. Neurologically he had mild clinical signs and focal EEG-abnormalities in the left fronto-temporal region, but CT, MRI, and SPECT showed no abnormality. Five years after the onset of amnesia there was no recovery of the retrograde memory deficit, but a PET (glucose) scan was normal and neuropsychological testing showed no deficits. An association with migraine has been reported for some non-classical amnesias, but this is the first case of selective retrograde amnesia in a patient with headache as a primary neurological diagnosis.
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PMID:Focal retrograde amnesia associated with vascular headache. 986 87

The transitory memory disturbance known as transient global amnesia (TGA) remains an enigma from a pathogenic point of view. In spite of its typical benign prognosis, TGA is a frightening experience for patients and their relatives. Moreover, a TGA episode usually leads to extensive investigation of patients in search of organic alterations that might be responsible for the event. Finally, TGA generates queries about therapeutic choices. In this review, we critically re-evaluate the evidence in support of and against the three main pathogenic hypotheses (i.e. ischemia, seizure discharge, and migraine), and we conclude that none of these appears completely convincing. Given the good prognosis and the lack of association with organic and instrumental abnormalities, we advance the hypothesis that TGA may be related to psychological disturbances causing transient alteration in brain metabolism and, consequently, amnesia. Our conclusion has relevant consequences in the evaluation of patients with TGA.
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PMID:Transient global amnesia: a review emphasizing pathogenic aspects. 1108 3

Pseudomigraine with pleocytosis (PMP) is an uncommon disease in Japan. The diagnostic criteria include at least one episode of transient neurological deficit accompanied or followed by migraine-like severe headache, cerebrospinal fluid (CSF) lymphocytosis, and normal neuroimaging. Both the etiology and the pathophysiology of PMP is not yet well defined. We report a 40-year-old man with a PMP-like syndrome. He came to our clinic because of severe throbbing headache and amnesia, and the examination showed CSF lymphocytosis of 23/mm3, a transient decrease of cerebral blood flow in the left thalamus. All the symptoms were completely resolved within 2 months.
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PMID:A patient of migraine-like headache with amnesia, pleocytosis and transient hypoperfusion of cerebral blood flow. 1609 86

Transient global amnesia is a clinically well defined syndrome, characterized by transient isolated epizodes of confusion with inability to acquire new data, repetitive quieries, retrograde amnesia and absence of other neurologic symptoms or signs. Eighteen patients who presented at admission the clinical picture of transient global amnesia were, after the examination, classified in three groups: patients with symptoms or signs of transitory focal ischemia, migraine group, and miscellaneous group. The transitory global amnesia in patients suffering from atherosclerotic changes of the vascular system is usually the first manifestation of transitory ischaemic attack pointing to the vascular insufficiency of the posterior cerebral regions as the cause of attack. The typical transient global amnesia is not a rare phenomenon, but it supposes the existence of the precipitating factors. Although its "pure" form is usually benign, the appearance of other factors such as cerebral neoplasms, involved in the aetiology of transient global amnesia, requires the complete clinical examination of each individual with these symptoms.
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PMID:[Transient global amnesia--possible aetiopathogenetic mechanisms]. 1629 27

Cortical spreading depression (CSD) is believed to be a putative neuronal mechanism underlying migraine aura and subsequent pain. In vitro and ex vivo/in vitro brain slice techniques were used to investigate CSD effects on the field excitatory postsynaptic potentials (fEPSP) and tetanus-induced long-term potentiation (LTP) in combined rat hippocampus-cortex slices. Induction of CSD in combined hippocampus-cortex slices in which DC negative deflections did not propagate from neocortex to hippocampus significantly augmented fEPSP amplitude and LTP in the hippocampus. Propagation of CSD to the hippocampus resulted in a transient suppression followed by reinstatement of fEPSP with amplitude of pre-CSD levels. LTP was inhibited when DC potential shifts were recorded in the hippocampus. Furthermore, CSD was induced in anaesthetized rats and, thereafter, hippocampal tissues were examined in vitro. LTP was significantly enhanced in hippocampal slices obtained from ipsilateral site to the hemisphere in which CSD was evoked. The results indicate the disturbances of hippocampal synaptic transmission triggered by propagation of CSD. This perturbation of hippocampal synaptic transmission induced by CSD may relate to some symptoms occurring during migraine attacks, such as amnesia and hyperactivity.
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PMID:Effect of cortical spreading depression on synaptic transmission of rat hippocampal tissues. 1655 74

The two main aetiologies of transient amnesia in the elderly are idiopathic transient global amnesia (TGA) and iatrogenic or toxic amnesia. Vascular and epileptic amnesia are less common. According to the literature, transient psychogenic amnesia, which is a frequent cause of amnesia at age 30 to 50, is very rare in the elderly. TGA is the prototypical picture of transient amnesia. It occurs more often after age 50, with no identified cause, even if some authors accept emotional stress or minor head trauma as occasional precipitants. The mechanism of TGA remains a matter of discussion. It may be the consequence of a spreading depression similar to that described in migraine with aura, but other arguments support an ischemic mechanism. Iatrogenic amnesias are mainly caused by benzodiazepines (BZs) or anticholinergics. The former may occur in a non-anxious subject, who is not a usual consumer of BZ and takes a single dose. The latter are more often due to a hypersensitivity to anticholinergic drugs, in particular in patients presenting with a covert, incipient Alzheimer's disease. A vascular origin must be considered when amnesia is accompanied by other neurological symptoms, and when the regression of the amnesic disorder is slow, lasting several days. It results from lesions involving various mechanisms and locations, mainly subcortical. Partial seizures, most often mesio-temporal, more rarely frontal, may be the cause of transient amnesia in the elderly, in the absence of a past history of epilepsy. The red flag supportive of an epileptic origin is the repetition of stereotyped amnesic episodes. EEG demonstration of seizures may be difficult and the response to antiepileptic drugs effective on partial seizures is usually good.
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PMID:[Transient amnesia in the elderly]. 1655 16

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


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