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)

We prospectively studied 19 children with severe hypertension to evaluate the spectrum of radiological changes, severity and reversibility of this entity. All of them were subjected to clinical and biochemical evaluation, followed by magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). Headache was seen in 17 children, 13 had confusion and drowsiness, 12 had nausea and vomiting, 10 patients had visual disturbances, seizure and dyspnoea. Only two had focal neurological deficit (one with right facial palsy and another with right lateral rectus palsy). Of these 19 children, 15 patients had hypertensive retinopathy and four had normal fundi. The positive MRI findings in 17/19 patients were: bilateral leukoencephalopathic changes in occipitoparietal region (9/17), diffuse white/grey matter lesion (3/17) patients, brain stem hyperintensity (2/17) and haemorrhagic lesions (3/17). On MRA, 12/19 patients had attenuation of cerebral arteries of different degree. On follow up, MRI findings resolved in all except three patients. All patients had normal MRA on follow up, except one with persistent minimal attenuation of middle cerebral artery and another had spasm in anterior, middle and posterior cerebral arteries. The intracranial abnormalities in these patients with severe hypertension were reversible in many of the cases after control of blood pressure was achieved. We therefore conclude that severe hypertension may lead to leuoencephalopathy, which had a wide radiological spectrum. A better understanding of this complex syndrome may obviate unnecessary investigations and allow management of associated problems in prompt and appropriate ways.
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PMID:Spectrum of radiological changes in hypertensive children with reversible posterior leucoencephalopathy. 1739 98

Coexistence of hemifacial spasm (HFS) and trigeminal neuralgia (TN) is a rare entity known as painful tic convulsif (PTC). Here, we present a case of right-sided HFS after which left TN developed, which is an unusual form of PTC. Both disorders were caused by bilateral vascular compression of the cranial nerves and successfully treated with botulinum toxin and carbamazepine. As PTC is benign in nature and can be treated with botulinum toxin, neuroradiological investigations should be performed for an accurate aetiological diagnosis, particularly in young patients with atypical disease manifestations.
J Headache Pain 2007 Sep
PMID:An unusual case of vascular loop syndrome. 1790 34

We report a 3-year-6-month-old boy with chordoid meningioma in the foramen magnum. Chordoid meningioma represents between 0.5 and 1.0% of all meningiomas, and it is frequently located in the supratentorial region. The patient started with an episode of instability, falls, and headache; after which, he developed cuadriparesis, cervical pain, and neck stiffness, which slightly improved after medical treatment, so he was referred to our hospital. Physical examination revealed left hemiparesis and cervical muscle spasm with left torticollis. Magnetic resonance imaging (MRI) demonstrated an intradural-extramedullary well-circumscribed, homogeneous enhancing mass, in the anterior part of the foramen magnum with cervical extension. The operative technique was the extreme-lateral craniocervical retrocondylar approach with total removal and dural coagulation. Histopathological examination demonstrated a chordoid meningioma, with meningotelial basophilic mucoid chordoma-like component in 80% of the tissue. The immunohistochemical stains were positive to epithelial membrane antigen, vimentin, and S-100 protein. At 10 months follow-up, the patient showed improvement in his neurological deficit with physical rehabilitation, and motor response in his extremities are now normal; neck stiffness with cervical spasm disappeared postoperatively. MRI showed no residual tumor. To our knowledge, this is the first report of a chordoid meningioma on the foramen magnum in a child.
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PMID:Chordoid meningioma of the foramen magnum in a child: a case report and review of the literature. 1821 97

The role of central versus peripheral mechanisms has always been questioned while explaining the etiopathogenesis of chronic tension type headache (CTTH). The following study was done to study the role of muscle spasm in CTTH. 15 patients of CTTH and 7 age matched controls were included in the study and their m. temporalis EMG was recorded for one minute each during rest, mental activity and maximal voluntary contraction and subjective pain scoring was done by visual analogue scale. The results revealed significant overactivity of m.temporalis in CTTH patients at rest when compared with control subjects (P = 0.01 and 0.03 left and right side respectively). After respective interventions namely non steroidal anti inflammatory drugs, botulinum toxin injections and yogic life style course, the EMG records revealed decrease in the mean EMG amplitude of m. temporalis during rest and mental activity more significantly after yoga based interventions (P = 0.03) and subjective pain scores decreased from 7.00 +/- 2.10 to 2.00 +/- 1.26 (P = 0.02) supporting the beneficial effect of such non invasive techniques.
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PMID:Role of temporalis muscle over activity in chronic tension type headache: effect of yoga based management. 1847 87

Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum as a complex of proteins containing the neurotoxin itself and other nontoxic proteins. Activation of the neurotoxin occurs upon proteolytic cleavage into the heavy and light chains. This di-chain moiety is essential for neurotoxin and each chain is playing a unique role; the heavy chain mediates neurospecifics cell binding and entry, whereas the light chain, a protease, catalyzes the cleavage and inactivation of neuronal proteins that mediate neurotransmitter release. There are seven BoNT serotypes (A,B,CI,D,E,F, and G), all of which inhibit acetylcholine release, though their intracellular target proteins, the characteristics of their actions, and their potencies vary substantially. BoNT type A has been the most widely studied and applied serotype for therapeutic purposes. It has been a mainstay in the treatment of cervical dystonia, blepharospasm, and hemifacial spasm for years. BoNT has more recently emerged as an increasingly important therapeutic option in the clinical management of a broad array of conditions, including other focal dystonias, spasticity, cerebral palsy, equinovarus, gastrointestinal (GI) and urogenital disorders, hypersecretory disorders, facial lines due to hyperfunctional facial muscles and recently, musculoskeletal pain disorders and headache.
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PMID:[Mechanism of therapy effects by botulinum neurotoxin]. 1854 57

Surgical sphincterotomy reduces anal tone and sphincter spasm and promotes ulcer healing. Because the surgery is associated with the side effect of faecal incontinence, pharmacological agents to treat chronic anal fissure have been explored recently. Glyceryl trinitrate (GTN) ointment (0.2%) has an efficacy of up to 68% in healing chronic anal fissure, but it is associated with headache as the major and most common side effect. Though botulinum toxin injected into the anal sphincter healed over 80% of chronic anal fissures, it is more invasive and expensive than GTN therapy. Diltiazem ointment achieved healing of chronic anal fissure comparable to 0.2% GTN ointment but was associated with fewer side effects. Other drugs that have been tried are lidocaine, the alpha-adrenergic antagonist indoramin, and the potassium channel opener minoxidil.
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PMID:Recent advances in the pharmacotherapy of chronic anal fissure: an update. 1865 16

The protein botulinum neurotoxin A (BoNT/A) is one of seven distinct neurotoxins produced by Clostridium botulinum. BoNT/A blocks cholinergic synapses with an extremely high specificity and potency. Appropriately purified and diluted, BoNT/A serves as a reliable and well tolerated drug that is applied by local injection.The efficacy of BoNT/A is evident in the symptomatic therapy of disorders in which muscular hyperactivity plays a prominent role, such as focal dystonias and hemifacial spasm; in these disorders, BoNT/A is considered first-line therapy. BoNT/A is also beneficial in the treatment of both adults and children with spasticity of various causes. The pain that frequently accompanies these conditions is effectively reduced by BoNT/A. A genuine analgesic effect for BoNT/A unrelated to skeletal muscle spasmolysis has been suggested on the basis of in vitro and in vivo (animal) data. However, studies in humans designed to detect such an effect were negative, as were controlled studies of BoNT/A in patients with primary headache disorders.BoNT/A also acts on cholinergic synapses of the autonomic nervous system, and injection of BoNT/A into salivary glands significantly decreases the production of saliva. This may be beneficial for patients with Parkinson's disease, in whom the excessive production of saliva may be problematic.Overall, BoNT/A has been confirmed as an efficacious, predictable and well tolerated drug in an ever-increasing number of neurological disorders.
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PMID:Use of botulinum toxin A in adult neurological disorders: efficacy, tolerability and safety. 1869 73

Anal fissure is a small linear tear in the lining of the distal anal canal below the dentate line. Treatment is aimed at reducing internal sphincter spasm. This can be achieved with surgery (lateral internal sphincterotomy) or pharmacological sphincterotomy applying topical medication, which relaxes the sphincter muscle. Glyceryl trinitrate is the most widely used topical agent. This is a nitric oxide donor which reduces the increased anal canal pressure caused by the hypertonic internal anal sphincter, improving anodermal blood flow. Although headache is a frequent side-effect, it is usually transient and glyceryl trinitrate does not seem to have any long-term adverse effects.
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PMID:[The role of glyceryl trinitrate in the treatment of anal fissure]. 1879 8

Nimodipine is a 1,4-dihydropyridine-derivative Ca(2+)-channel blocker developed approximately 30 years ago. It is highly lipophilic, crosses the blood-brain barrier, and reaches brain and cerebrospinal fluid. Early treatment with nimodipine reduces the severity of neurological deficits resulting from vasospasm in subarachnoid haemorrhage (SAH) patients. In SAH, nimodipine reduced spasm-related deficits of all severities, but no spasm-unrelated deficits. This paper has reviewed preclinical studies on the influence of nimodipine in various animal models of cerebral ischemia, with particular attention toward investigations published in the last 10 years. These studies further support the main indication of nimodipine, by clarifying some mechanisms of the anti-ischemic activity of the compound. Papers reporting a possible role of nimodipine in epileptogenesis were also examined. Clinical studies on nimodipine were grouped into subarachnoid hemorrhage, acute ischemic stroke, cerebral ischemia without stroke, dementia disorders, and migraine. Clinical investigations have shown that the drug improves neurological outcome by reducing the incidence and severity of ischemic deficits in patients with SAH from ruptured intracranial berry aneurysms regardless of their post-ictus neurological condition. No relevant effects of treatment with nimodipine were reported for acute ischemic stroke, cerebral ischemia without stroke, and migraine, except than for cluster headache. The less pronounced cardiovascular effects of nimodipine compared to other dihydropyridine-type Ca(2+)-channel blockers probably accounts for its use out of label for treating patients affected by chronic cerebral ischemia and vascular cognitive impairment. However, the blood pressure-lowering effects of nimodipine should not be minimized, as clinical studies have documented lowering blood pressure in small groups of patients, including cases of withdrawn due to pronounced hypotension induced by nimodipine administration. In the area of vascular cognitive impairment, short-term benefits of nimodipine do not justify its use as a long-term anti-dementia drug, and benefits obtained in elderly patients affected by subcortical vascular dementia require to be confirmed by other groups and in larger scale trials. In conclusion, nimodipine is a safe drug with an important place in pharmacotherapy and with the main documentation for reduction in the severity of neurological deficits resulting from vasospasm in SAH patients.
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PMID:Nimodipine and its use in cerebrovascular disease: evidence from recent preclinical and controlled clinical studies. 1902 Oct 25

Cerebral phaeohyphomycosis is a fungal infection of the brain typically caused by Cladophialophora bantiana, Exophiala dermatitidis, and Rhinocladiella mackenziei, all of which belong to the order Chaetothyriales. The disease results in black, necrotic brain tissue, black pus, and black cerebrospinal fluid. Pathogens usually reach the brain through the bloodstream or lymphatic fluid and occasionally through direct spreading or accidental inoculation. Patients can present with hemiparesis, tonic spasm, headache, fever, sensory variation, cerebral irritation, and even psychotic behavioural changes. Radiological images are characterised by ring-enhanced signs and hyperdense and hypodense lesions. Pathological features frequently include black-to-brown necrotic tissue or dark-coloured pus, granulomatous inflammation, giant cell vasculitis, and pigmented fungal elements, which are easily seen on a direct potassium hydroxide smear, a rapid method for diagnosis. Black fungi can be cultured from a biopsy specimen. Combined antifungal chemotherapy, surgical debridement, and careful immunological interventions are strongly recommended to eradicate these intractable infections.
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PMID:Cerebral phaeohyphomycosis--a cure at what lengths? 1946 77


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