|1.||Strupp, Michael: 6 articles (07/2013 - 04/2007)|
|2.||Brandt, Thomas: 5 articles (07/2013 - 04/2007)|
|3.||Baloh, Robert W: 5 articles (01/2012 - 02/2002)|
|4.||Jen, Joanna C: 4 articles (02/2008 - 04/2002)|
|5.||Frontali, M: 4 articles (01/2003 - 01/2000)|
|6.||Spacey, Sian D: 3 articles (01/2013 - 08/2004)|
|7.||Tournier-Lasserve, E: 3 articles (05/2011 - 02/2001)|
|8.||Kullmann, D M: 3 articles (11/2009 - 02/2001)|
|9.||Baloh, R W: 3 articles (12/2003 - 10/2001)|
|10.||Jodice, C: 3 articles (01/2003 - 01/2000)|
|1.||Migraine with Aura (Familial Hemiplegic Migraine)
05/01/2015 - "Eight reported patients have a deletion also encompassing CACNA1A, haploinsufficiency of which causes episodic ataxia type 2 or familial hemiplegic migraine. "
01/01/2015 - "The other two disorders are Episodic Ataxia type 2 (EA2), and Familial Hemiplegic Migraine type 1 (FHM1). "
12/01/2010 - "Patients with familial hemiplegic migraine were not significantly different from either controls or patients with episodic ataxia type 2. Together, these findings indicate that patients with episodic ataxia type 2 have an excessive increase in motor cortex excitability following a strong facilitatory input. "
12/01/2010 - "We tested this hypothesis in patients with episodic ataxia type 2 (n = 6), patients with familial hemiplegic migraine (n = 7) and healthy controls (n = 13). "
12/01/2010 - "Thus, we hypothesized that channel dysfunction in episodic ataxia type 2 and familial hemiplegic migraine may impair the ability to adjust cerebral excitability after facilitatory events. "
|2.||Cerebellar Diseases (Cerebellar Syndrome)
11/01/2012 - "In addition, the profiles of three participants with a rare autosomal dominant cerebellar disease were assessed (episodic ataxia type 2, EA-2). "
01/01/2010 - "Episodic ataxia type 2 (EA2) is characterized by paroxysmal bouts of ataxia and progressive cerebellar dysfunction. "
04/01/2006 - "Episodic ataxia type 2 (EA2) is an inherited autosomal dominant disorder related to cerebellar dysfunction and is associated with mutations in the pore-forming alpha(1A)-subunits of human P/Q-type Ca(2+) channels (Cav2.1 channels). "
04/01/2006 - "Downbeat nystagmus (DBN) is caused by cerebellar disease, which includes structural lesions affecting the flocculus and paraflocculus, and calcium channelopathies, such as episodic ataxia type 2 (EA2), for which a mouse model and effective treatment is available. "
04/01/2013 - "The reversible potassium channel blocker 4-aminopyridine is effective in the treatment of numerous cerebellar dysfunctions, such as episodic ataxia type 2 and downbeat nystagmus syndrome. "
09/08/2001 - "We aimed to determine whether the P/Q-type Ca(2+) channel is associated with both epilepsy and episodic ataxia type 2 in human beings. "
01/12/2002 - "Human epilepsy, episodic ataxia type 2, and migraine."
03/01/2003 - "Acetazolamide, which is thought to ameliorate ion channel function, was shown effective in familial hemiplegic migraine and episodic ataxia type 2, both of which are associated with mutations of the neuronal Ca2+-channel gene CACNA1A, as well as in aura status. "
12/01/2001 - "Here, we reviewed several channelopathies including spinocerebellar ataxia type 6, familial hemiplegic migraine, episodic ataxia type 2, familial hypokalemic periodic paralysis, congenital myotonia, malignant hyperthermia, epilepsy, Gitelman syndrome and Lambert-Eaton syndrome."
01/01/2001 - "(1) Sodium channelopathies: familial generalized epilepsy with febrile seizures plus, hyperkalemic periodic paralysis, paramyotonias, hypokalemic periodic paralysis; (2) potassium channelopathies: benign infantile epilepsy, episodic ataxia type 1; (3) calcium channelopathies: episodic ataxia type 2, spinocerebellar ataxia type 6, familial hemiplegic migraine, hypokalemic periodic paralysis, central core disease, malignant hyperthermia syndrome, congenital stationary night blindness; (4) chloride channelopathies: myotonia congenitas; (5) ACh receptor channelopathies: autosomal dominant frontal lobe nocturnal epilepsy, congenital myasthenic syndromes; (6) glycine receptor channelopathies: hyperekplexia. "
|4.||Vestibular Neuronitis (Vestibular Neuritis)
01/01/2013 - "Considerable advances have been made in the treatment of vertigo disorders in the last 10 years, e.g., cortisone for the treatment of acute vestibular neuritis, betahistine as a high-dosage, long-term treatment for Menière's disease, carbamazepine to treat vestibular paroxysmia and aminopyridine for downbeat nystagmus and episodic ataxia type 2."
07/01/2009 - "In vestibular neuritis, recovery of the peripheral vestibular function can be improved by oral corticosteroids; in Menière's disease, there is first evidence that high-dose, long-term administration of betahistine reduces attack frequency; carbamazepine or oxcarbamazepine is the treatment of first choice in vestibular paroxysmia, a disorder mainly caused by neurovascular cross-compression; the potassium channel blocker aminopyridine provides a new therapeutic principle for treatment of downbeat nystagmus, upbeat nystagmus, and episodic ataxia type 2."
03/01/2011 - "Examples of such causal therapy include aminopyridines for downbeat nystagmus and episodic ataxia type 2; carbamazepine for vestibular paroxysmia, paroxsymal dysarthria and ataxia in multiple sclerosis, and superior oblique myokymia; betahistine, dexamethasone, and gentamicin for Menière's disease; gabapentin and memantine for different forms of acquired and congenital nystagmus; corticosteroids for acute vestibular neuritis and Cogan's syndrome; metoprolol and topiramate for vestibular migraine; and selective serotonin reuptake inhibitors such as paroxetine for phobic postural vertigo. "
|5.||Low Vision (Subnormal Vision)
02/01/2015 - "PHARMACOLOGICAL TREATMENT: Depending on the pathophysiology of different types of nystagmus, several drugs were effective in clinical application (off-label use): (i) gabapentin (non-selective GABAergic and anti-glutamatergic effect): up to 2400 mg/d in infantile nystagmus, acquired pendular nystagmus and oculopalatal tremor, (ii) nemantine (anti-glutamatergic effect): dosage up to 40 mg/d in infantile nystagmus, also in acquired pendular nystagmus and oculopalatal tremor, (iii) baclofen (GABA-B-receptor agonist): 3 × 5-10 mg/d in periodic alternating nystagmus and in upbeat nystagmus, (iv) 4-aminopyridine (non-selective blocker of voltage-gated potassium channels): 3 × 5 mg/d or 1-2 × 10 mg Fampridin in downbeat nystagmus and upbeat nystagmus, (v) acetazolamide (carbonic anhydrase inhibitor): in hereditary episodic ataxia type 2. OPTICAL DEVICES: (i) Contact lenses are used in infantile nystagmus in order to overcome negative effects of eye glasses in abnormal head posture, lateral gaze, and higher refractive errors, (ii) spectacle prisms are useful to induce an artificial exophoria (base-out prisms) or to shift an excentric null zone (base in direction of head posture) of infantile nystagmus with abnormal head posture, (iii) low vision aids may be necessary and should be prescribed according to magnification requirements."
|2.||Potassium Channels (Potassium Channel)
|3.||4-Aminopyridine (4 Aminopyridine)
|5.||Adrenal Cortex Hormones (Corticosteroids)
|6.||Ion Channels (Ion Channel)
|9.||GABA-B Receptor Agonists
|10.||Voltage-Gated Potassium Channels (Voltage-Gated Potassium Channel)
|5.||Drug Therapy (Chemotherapy)