Catatonia due to central pontine and extrapontine myelinolysis: case report

Chalela, Julio A.; Kattah, Jorge

doi:10.1136/jnnp.67.5.692

Cited by 35 publications

(9 citation statements)

References 4 publications

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“…Normal neuroimaging findings at the beginning of CPM may suggest a psychogenic etiology [5]. Common psychiatric manifestations include agitated delirium, a pseudobulbar state with pathological laughing and crying, akinetic mutism and catatonia [36]. Other neuropsychological deficits have been observed with regard to attention, concentration, short-term memory, visual motor and fine motor speeds and learning ability [42].…”

Section: Clinical Picture and Diagnosismentioning

confidence: 99%

Central Pontine Myelinolysis

Lampl

Yazdi²

2002

Eur Neurol

225

143

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Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with demyelination of other areas of the central nervous system (CNS). The term ‘osmotic demyelinization syndrome’ is used for pontine and extrapontine myelinolysis. In this paper, we are concerned with CPM although the extrapontine one is based on the same pathogenesis. Both share the diagnostic methods, and their prevention and therapy are the same. The etiology and pathogenesis of this disorder are unclear and will be discussed. However, almost all cases of CPM are related to severe diseases. Chronic alcoholism is still the most common underlying condition of CPM patients. In the literature, 174 cases of CPM have been reported in alcoholics since 1986, which is equivalent to an incidence of 39.4%. Likewise, 95 cases of CPM following the correction of hyponatremia have been documented since 1986 (21.5%). The role of hyponatremia and its correction will be outlined in the discussion of the pathogenesis of CPM. The third largest group of CPM cases are liver transplant patients (17.4%), with the development of CPM being attributed to the immunosuppressive agent cyclosporine in particular. Depending on the involvement of other CNS structures, the clinical picture can vary considerably. The large-scale introduction of magnetic resonance imaging has increasingly facilitated the antemortem diagnosis of CPM, although the radiological findings lag behind and do not necessarily correlate with the clinical picture. As yet, there is no specific therapy of choice. A number of therapeutic approaches have been tested and although they have not been compared with regard to their rate of success, they have all led to a substantial improvement in the prognosis of CPM.

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Section: Clinical Picture and Diagnosismentioning

confidence: 99%

Central Pontine Myelinolysis

Lampl

Yazdi²

2002

Eur Neurol

225

143

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“…However, occasional reports of Parkinsonism as the most prominent clinical feature in extrapontine myelinolysis with or without central pontine involvement have been published in recent years [3,5,9,11,13]. To our knowledge, catatonia was reported in only one case [2]. We describe in this report a case of extrapontine myelinolysis following rapid correction of hyponatremia presenting as catatonia and Parkinsonism.…”

mentioning

confidence: 72%

Catatonia and Parkinsonism due to extrapontine myelinolysis following rapid correction of hyponatremia

Koussa

Nasnas

2003

Journal of Neurology

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“…Esant ðiems simp to mams ir nor ma liems neu ro vi zu a li niams ty ri mams OM pra dþio je, ga li ma pa galvo ti apie psi chiat ri nae li gà [4]. Daþ nai psi chi kos su tri ki mai ma ni fes tuo ja aþi tuo tu de ly ru, pseu do bul ba ri ne bûk le su pa to lo gi niu juo ku ar ver ki mu, aki me ti niu mu tiz mu, ka tato ni ja [30]. Ki ti ste bë ti neu rop si cho lo gi niai de fi ci tai -dë -me sio, kon cen tra ci jos, trum pa lai kës at min ties ir mo ky mosi su tri ki mai [31].…”

Section: Klinikiniai Simptomaiunclassified

“…Ki ti ste bë ti neu rop si cho lo gi niai de fi ci tai -dë -me sio, kon cen tra ci jos, trum pa lai kës at min ties ir mo ky mosi su tri ki mai [31]. Ðie simp to mai ga li ið lik ti il ges ná lai kà, ta èiau jie ne bû ti nai ko re liuo ja su ra dio lo gi niais ir neu ro logi niais ra di niais [30].…”

Section: Klinikiniai Simptomaiunclassified

“…Ka dan gi OM kli ni ki niai simp to mai ir ra dio lo gi niai vaiz dai tar pu sa vy je ne ko re liuo ja [30,33], to dël sun ku nu spë ti klini ki nës ei gos vys ty mà si ir prog no zae. R. Ab bott su ko le gomis, ið ty rae 34 OM pa cien tus, pra ne ði me pa skel bë, kad mirtin gu mas tarp jø bu vo 6 %, 30 % -simp to mai ið ny ko vi sið -kai, 32 % -li ko tam tik rø simp to mø, ta èiau jie bu vo ne priklau so mi nuo ki tø as me nø.…”

Section: Prognozëunclassified

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Osmotic myelinolysis: literature review and case report

Rutkauskaitė

Klimašauskienė

2018

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Vilniaus universitetas, Medicinos fakultetas, Klinikinës medicinos institutas, Neurologijos ir Neurochirurgijos klinika ÁVADASOs mo si në mie li no li zë (OM) yra re tas ir ûmus de mie li nizuo jan tis su sir gi mas. 1959 m. R. D. Ad ams su ko le go mis [1] pir mie ji ap ra ðë cen tri nae til to mie li no li zae (CTM), ku rià diag no za vo al ko ho liu pik tnau dþiau jan tiems ir pras tai be simai ti nan tiems as me nims. Vë liau nu sta ty ta, kad iden tið ki pa to lo gi niai po ky èiai ga li pa si reikð ti taip pat uþ til to ri bø, jie pa va din ti eks tra pon ti ni ne mie li no li ze (EPM). Vyk dant moks li nius ty ri mus, ið aið kin tas ry ðys tarp OM ir grei tos nat rio ko rek ci jos pa cien tams, ser gan tiems hi po nat re mi ja. EPIDEMIOLOGIJATiks lus OM pa pli ti mas në ra þi no mas. Pir mie ji duo me nys apie OM gau ti au to psi jø me tu. M. Vic tor ir R. Lau re no apra ðy to je 3 548 su au gu siø jø au to psi jø ana li zë je OM bû din gi pa þei di mai ras ti 0,25 % at ve jø [2]. Ki ta me moks li nia me dar be bu vo ið ana li zuo ta 3 000 mi ru siø jø sme ge nø, 0,005 % jø nu sta ty ta asimp to më CTM [3]. Au to psi jø ana li zë je didþiau sias OM pa pli ti mas, nu sta ty tas 30-50-ai siais gy ve nimo me tais, dau giau bû din gas vy rams [4], ta èiau pa to lo giniai po ky èiai pa ste bë ti ir vai kams [5,6]. A. Gocht ir ko le gø [7] au to psi jø stu di jo je ið nag ri në ti 58 OM kli ni ki niai at ve - San trau ka. Cen tri në til to mie li no li zë api bû di na ma kaip os mo si nës mie li no li zës sin dro mas, daþ niau siai ið si vys tan tis kaip kom pli ka ci ja po grei tos hi po nat re mi jos ko rek ci jos. Til to mieli no li zë skirs to ma á cen tri nae til to mie li no li zae ir eks tra pon ti ni nae mie li no li zae. Hi po nat re mi ja daþ nai nu sta to ma pa cien tams, ku rie pik tnau dþiau ja al ko ho liu, pras tai mai ti na si, var to jant tam tik rus vais tus, taip pat ser gant ke pe nø li go mis, esant pa ki tu siai an ti diu re zi nio hor mo no sin te zei, ant inks èiø ne pa kan ka mu mui. Yra ke le tas pa to fi zio lo gi niø me cha niz mø, pa aið kinan èiø os mo si nës mie li no li zës ið si vys ty mà. Bû din ga dvi fa zë li gos ei ga. Pir mie ji simp to mai yra en ce fa lo pa ti ja ir (ar) trau ku liø prie puo liai, pa si reið kae dël hi po nat re mi jos, vë liau ste bi mas at si sta ty mas nor mo nat re mi jos me tu ir po ke liø die nø -pa blo gë ji mas, ga lin tis pa si reikð ti þi -di ni ne neu ro lo gi ne simp to ma ti ka, psi chi kos ir el ge sio su tri ki mais. Anks èiau siai bû din gus pa ki ti mus sme ge ny se ga li ma pa ste bë ti mag ne ti nio re zo nan so to mog ra fi jos DWI re þi mu. Patvir tin tø os mo si nës mie li no li zës gy dy mo re ko men da ci jø në ra, ta èiau li te ra tû ro je ap ra ðo mi sëk min gi at ve jai, pa cien tus gy dant ti rot ro pi nà ið ski rian èiu hor mo nu, gy do mo sio mis afe re zë -mis, gliu ko kor ti koi dais, in tra ve ni niu imu nog lo bu li nu. Os mo si nës mie li no li zës ga li ma ið -veng ti, hi po nat re mi jos me tu nat rio kon cen tra ci j...

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Catatonia due to central pontine and extrapontine myelinolysis: case report

Cited by 35 publications

References 4 publications

Central Pontine Myelinolysis

Central Pontine Myelinolysis

Catatonia and Parkinsonism due to extrapontine myelinolysis following rapid correction of hyponatremia

Osmotic myelinolysis: literature review and case report

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