Treatment of palatal myoclonus with sumatriptan

Scott, Burton L.; Evans, Randolph W.; Jankovic, Joseph

doi:10.1002/mds.870110628

Cited by 37 publications

(23 citation statements)

References 38 publications

(13 reference statements)

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“…In another report, an acute onset of depressive symptoms was described after treatment with sumatriptan for migraine, in a patient with a history of recurrent depression (LaPorta 1995). It has been postulated that, despite its poor penetration of the blood-brain barrier, sumatriptan might exert central cerebral e¤ects in areas not shielded by the blood-brain barrier, such as the area postrema, choroid plexus, dorsal root ganglia or hypophyseal circulation (Scott et al 1996) or in subjects in whom the blood-brain barrier is less e¦cient due to the disease process. Selective 5-HT 1D receptor agonists or antagonists with better penetrating properties for the blood-brain barrier are warranted, to explore further the role of the 5-HT 1D receptors in the pathophysiology of OCD.…”

Section: Discussionmentioning

confidence: 97%

Sumatriptan (5-HT 1D receptor agonist) does not exacerbate symptoms in obsessive compulsive disorder

Pian¹,

Westerberg²,

Megen³

et al. 1998

Psychopharmacology

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The non-selective serotonin (5-HT) receptor agonist meta-chlorophenylpiperazine (mCPP) has been reported to elicit symptoms in patients with obsessive compulsive disorder (OCD). MK-212, another non-selective 5-HT receptor agonist, does not seem to induce obsessive compulsive symptoms in OCD patients. The major pharmacological difference between mCPP and MK-212 is their affinity for the 5-HT(ID) receptor. The aim of this study was to explore the role of the 5-HT(ID) receptor in the pathophysiology of OCD, by using a challenge paradigm with the selective 5-HT(ID) receptor agonist sumatriptan (Imigran). A randomized, double-blind, placebo-controlled crossover challenge with sumatriptan (100 mg PO) was performed in 15 OCD patients. Neither the obsessive compulsive symptoms nor mood or anxiety symptoms changed significantly following sumatriptan administration as compared to placebo. Sumatriptan did induce a significant increase in plasma growth hormone (GH) levels. In the present study, no indication were found for the role of the 5-HT(ID) receptor in the pathophysiology of OCD. It should be noted, however, that sumatriptan does not readily pass the blood-brain barrier. Selective 5-HT(ID) receptors with better brain penetrating properties may shed more light on the role of this 5-HT receptor subtype in OCD.

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Section: Discussionmentioning

confidence: 97%

Sumatriptan (5-HT 1D receptor agonist) does not exacerbate symptoms in obsessive compulsive disorder

Pian¹,

Westerberg²,

Megen³

et al. 1998

Psychopharmacology

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“…Many drugs were tried and the only effective was clonazepan. In these two reports the patients with SPM did not respond to the administration of sumatriptan 4,11 .…”

Section: Fig 2 Electromyography (Sumatriptan In the Case 1)mentioning

confidence: 92%

“…Scott et al in 1996 reported the treatment of palatal myoclonus in 2 patients, one with primary palatal myoclonus-PPM (showed a positive response) and the other with secondary palatal myoclonus (SPM) that showed no response to the administration of sumatriptan 4 . Gambardela et al in 1997 reported a case after remove of intestinal lymphoma which showed no response to the use of sumatriptan 11 .…”

Section: Fig 2 Electromyography (Sumatriptan In the Case 1)mentioning

confidence: 99%

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Palatal myoclonus: report of two cases

Fabiani

Teive

Sá

et al. 2000

Arq. Neuro-Psiquiatr.

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-We describe two cases of palatal myoclonus (PM), one essential and another secondary to a stroke. Case 1: a 64 years old female who developed clicking sounds in both ears after a stroke and three years later on noticed a progressive involuntary movement of the throat associated with rhythmic contractions of the soft palate, muscles of tongue and throat. MRI showed an ischemic area in brainstem. The patient had a partial response to the use of sumatriptan 6 mg subcutaneously. Case 2: a 66 years old female who began with ear clicking at left ear that worsed slowly associated with tinnitus and arrhythmic movements of soft palate and an audible click at left ear. Brain MRI was normal; audiometry showed bilateral neurosensory loss. She was prescribed clonazepan 1 mg daily with complete recovery. Primary and secondary palatal myoclonus share the same clinical features but probably have different pathophysiological underlying mechanisms.KEY WORDS: palatal myoclonus, sumatriptan, clonazepan. Mioclonia palatal: relato de dois casosRESUMO -Descrevemos dois casos de mioclonia palatal (MP), um essencial e o outro secundário a acidente vascular cerebral (AVC). Caso1: mulher de 64 anos que desenvolveu cliques audíveis em ambos os ouvidos após um AVC e que três anos depois começou a apresentar movimentos involuntários do pálato, músculos do língua e garganta. A ressonância magnética (RNM) mostrou áreas de isquemia no tronco cerebral. A paciente apresentou resposta parcial e não duradoura ao uso subcutâneo de 6 mg de sumatriptano. Caso 2: mulher de 66 anos, com cliques audíveis no ouvido esquerdo que pioraram progressiva e lentamente associados com tinitus e movimentos mais ou menos rítmicos do pálato mole. A RNM encefálica era normal. A audiometria mostrou perda neurossensorial bilateral. Foi medicada com 1,0 mg de clonazepan diariamente com completa recuperação. MP primária e secundária compartilham das mesmas características clínicas, mas evidências sugerem que se devam a diferentes mecanismos fisiopatológicos. PALAVRAS-CHAVE: mioclonia palatal, sumatriptano, clonazepan.Palatal myoclonus (PM) is a form of segmental myoclonus. It is an uncommon, rhythmic, "shock-like" involuntary movement of the muscles of soft palate, throat and other structures derived from the branchial arcs 1-3 . Some authors prefer to call it palatal tremor 3 . Jankovic suggests that the most correct term shall be PM 4 . Although it is a rare condition , it is well established that the anatomic structures involved in the process are almost always in the inferior olivary nucleus -that show an hypertrophic degeneration [1][2][3]5,6 .

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“…Thus far no evidence was found in animal research that sumatriptan can pass the blood-brain barrier, although it is possible that sumatriptan acts centrally via places where the protective effect of the blood-brain barrier is not present (Scott et al 1996). Different studies found an increase in plasma GH levels in healthy subjects after the use of sumatriptan (Boeles et al 1997;Sciberras et al 1997).…”

Section: Introductionmentioning

confidence: 95%

Zolmitriptan (a 5-HT1B/1D receptor agonist with central action) does not increase symptoms in obsessive compulsive disorder

Boshuisen

Boer

2000

Psychopharmacology

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Treatment of palatal myoclonus with sumatriptan

Abstract: Segment 2. Vocal tics in the same patient 4 weeks after his second treatment with 3.75 units of botulinum toxin to each thyroarytenoid muscle. He reports a 50% decrease in scream volume and a 1040% decrease in scream frequency.

Cited by 37 publications

References 38 publications

Sumatriptan (5-HT 1D receptor agonist) does not exacerbate symptoms in obsessive compulsive disorder

Sumatriptan (5-HT 1D receptor agonist) does not exacerbate symptoms in obsessive compulsive disorder

Palatal myoclonus: report of two cases

Zolmitriptan (a 5-HT1B/1D receptor agonist with central action) does not increase symptoms in obsessive compulsive disorder

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