Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009676 (confusion)
 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cervicogenic headache (CH) originates from disorders of the neck but is recognized as a referred pain in the head. Primary sensory afferents from the cervical roots C1-C3 converge with afferents from the occiput and trigeminal afferents on the same second-order neuron in the upper cervical spine. Consequently, the anatomical structures innervated by the cervical roots C1-C3 are potential sources of CH. In normal volunteers, the painful stimulation of different anatomical structures of the neck produced headache. In CH, particular structures have been selectively anesthetized in order to identify possible sources of pain. In summary, CH can origin from different muscles and ligaments of the neck, from intervertebral discs,and, particularly, from the atlantooccipital, atlantoaxial, and C2/C3 zygapophyseal joints. Diagnosis of CH should adhere strictly to the published diagnostic criteria to avoid misdiagnosis and confusion with primary headache disorders such as migraine and tension type headache.
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PMID:[Pathophysiology and clinical manifestation of cervicogenic headache]. 1269 93

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

Prolonged hemiparetic migraine aura can cause diagnostic confusion and be mistaken for ischaemic stroke occurring during the course of a migraine--'migrainous infarction'. We report a case of prolonged hemiparesis occurring during the course of a migraine attack. Though initially confused with migrainous infarction, we suggest with sequential magnetic resonance imaging, magnetic resonance angiography, diffusion, perfusion images and magnetic resonance spectroscopy that the hemiplegia was not of vascular origin and that the patient had sporadic hemiplegic migraine. We hypothesize that the mechanisms of sporadic hemiplegic migraine probably lie at a cellular level, similiar to familial hemiplegic migraine.
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PMID:Imaging abnormalities in sporadic hemiplegic migraine on conventional MRI, diffusion and perfusion MRI and MRS. 1688 37

The central nervous system (CNS) is, after the peripheral nervous system, the second most frequently affected organ in mitochondrial disorders (MCDs). CNS involvement in MCDs is clinically heterogeneous, manifesting as epilepsy, stroke-like episodes, migraine, ataxia, spasticity, extrapyramidal abnormalities, bulbar dysfunction, psychiatric abnormalities, neuropsychological deficits, or hypophysial abnormalities. CNS involvement is found in syndromic and non-syndromic MCDs. Syndromic MCDs with CNS involvement include mitochondrial encephalomyopathy, lactacidosis, stroke-like episodes syndrome, myoclonic epilepsy and ragged red fibers syndrome, mitochondrial neuro-gastrointestinal encephalomyopathy syndrome, neurogenic muscle weakness, ataxia, and retinitis pigmentosa syndrome, mitochondrial depletion syndrome, Kearns-Sayre syndrome, and Leigh syndrome, Leber's hereditary optic neuropathy, Friedreich's ataxia, and multiple systemic lipomatosis. As CNS involvement is often subclinical, the CNS including the spinal cord should be investigated even in the absence of overt clinical CNS manifestations. CNS investigations comprise the history, clinical neurological examination, neuropsychological tests, electroencephalogram, cerebral computed tomography scan, and magnetic resonance imaging. A spinal tap is indicated if there is episodic or permanent impaired consciousness or in case of cognitive decline. More sophisticated methods are required if the CNS is solely affected. Treatment of CNS manifestations in MCDs is symptomatic and focused on epilepsy, headache, lactacidosis, impaired consciousness, confusion, spasticity, extrapyramidal abnormalities, or depression. Valproate, carbamazepine, corticosteroids, acetyl salicylic acid, local and volatile anesthetics should be applied with caution. Avoiding certain drugs is often more beneficial than application of established, apparently indicated drugs.
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PMID:Central nervous system manifestations of mitochondrial disorders. 1694 41

Confusional migraine (CM) is recognized as a kind of pediatric migraine equivalent. We report that a 10-year-old girl had repeated attacks of confusional state and of migraine with aura. She suffered from total of six CM attacks and migraine attacks with aura almost once a month. Therefore, sodium valproate (VPA) was initiated to prevent these attacks. They have been controlled after increasing her dosage to 600mg/day. The intracranial magnetic resonance angiography (MRA) during the last CM attack indicated narrowing of left middle and posterior cerebral arteries. However, MRA during the attack free period at 41-day follow-up showed normal vessels. Electroencephalograms showed severe slowing without seizure discharges during the CM attacks. This case indicates that VPA is an effective treatment for the prophylaxis of CM and migraine with aura. MRA is considered helpful for the diagnosis of this kind of migraine in children because of noninvasive neuroimaging.
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PMID:The efficacy of sodium valproate and a MRA finding in confusional migraine. 1697 24

(1) The first-line drug for prevention of migraines is propranolol: it is the most thoroughly evaluated treatment, and thus far no other drug has been found to be more effective. (2) Topiramate, an antiepileptic drug, is now also approved for migraine prevention. Only 3 out of 4 double-blind placebo-controlled trials showed that topiramate 100 mg/day was effective: on average, 46% of patients had a reduction of at least 50% in the frequency of migraines, compared to 23% of patients on placebo. Increasing the dose to 200 mg did not lead to better efficacy. (3) A double-blind trial versus propranolol failed to show that topiramate was as effective or better than propranolol. (4) Topiramate has numerous, frequent and sometimes serious adverse effects, mainly including neurosensory disorders (paraesthesias, language disorders, confusion) and gastrointestinal disturbances. (5) Topiramate treatment costs nearly 5 times more than propranolol. (6) In practice, the adverse effects of topiramate outweigh its efficacy in the prevention of migraine attacks.
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PMID:Topiramate: new indication. Migraine prevention: best avoided. 1698 25

Headache and migraine are common features in multiple sclerosis (MS) and can influence the diagnosis, radiological evaluation, treatment, and quality of life of these patients. Similarities in symptoms between patients with migraine and MS presenting with headache can lead to misdiagnosis. Likewise, MRI lesions which may be found in migraine patients without other neurological symptoms or signs may cause diagnostic confusion and patient anxiety. Studies addressing the pathophysiology of these comorbid conditions have not found a clear link, but brainstem lesions and inflammatory processes have been proposed. Management of de novo or treatment-induced headache in the MS patient is fairly straightforward if the physician is aware of the problem.
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PMID:Migraine in multiple sclerosis. 1753 46

In this report, a case with vitamin B12 deficiency showing a temporary confusion depending on the usage of naratriptan during the migraine attack was presented.
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PMID:Temporary confusion depending on the usage of naratriptan. 1807 30

Valproic acid (VPA) is used to manage a variety of conditions, including simple and complex absence seizure disorder, bipolar disorder, and migraine prophylaxis. The clinical manifestations of VPA overdose range in severity from mild confusion and lethargy to severe coma and death. The treatment of VPA toxicity is mainly supportive. There is no specific antidote or guidelines for managing VPA intoxication. Anecdotal reports describe the efficacy of naloxone and L-carnitine, but the data are insufficient to make strong conclusions. Various extracorporeal techniques for managing VPA toxicity have been described, but none has prevailed as standard therapy. We report a patient with VPA overdose who was treated successfully with hemoperfusion with activated charcoal and L-carnitine. The VPA level of the patient exceeded 1000 microg/mL and was normalized after 3 rounds of hemoperfusion. The patient was injected with L-carnitine at a maximum of 600 mg/kg per day for 5 days without complications.
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PMID:A case of hemoperfusion and L-carnitine management in valproic acid overdose. 1835 83

Hemiplegic migraine (HM) is a rare variety of migraine with aura characterized by the presence of a motor weakness during the aura. Hemiplegic migraine has two main forms according to the familial history: patients with at least one first- or second-degree relative who has aura including motor weakness have familial hemiplegic migraine (FHM); patients without such familial history have sporadic hemiplegic migraine (SHM). The prevalence of HM is one in 10,000 with FHM and SHM being equally frequent. Typical HM attacks include a motor weakness that is always associated with other aura symptoms, the most frequent being sensory, visual and speech disorders. In addition, basilar-type symptoms occur in up to 70% of the patients. Severe attacks may occur in FHM as well as in SHM with prolonged hemiplegia, confusion, coma, fever and seizures. The clinical spectrum also includes permanent cerebellar signs (nystagmus, ataxia, dysarthria) and less frequently various types of seizures and intellectual deficiency. FHM is the only variety of the autosomal dominant migraine and all three know genes encode ion-transporters. A genetic diagnosis is now possible by screening the three known genes involved in FHM (CACNA1A, ATP1A2 and SCNA1). Prognosis is usually good. Treatment is similar to approaches used in other varieties of migraine with aura, excepted for triptans that are contraindicated in MHF/MHS. Based on new pathophysiological insight, preventive treatments by various antiepileptic agents seem promising.
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PMID:[Familial and sporadic hemiplegic migraine]. 1840 71


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