Joaquim, Natércia

Martins, Cristiana

Mogildea, Mihail

Nzwalo, Hipolito

Soleiro, Jose

Varela, Miguel

Journal of Neurosciences in Rural Practice

English

Mihail Mogildea

Miguel Varela

Cristiana Martins

Natércia Joaquim

José Soleiro

Hipólito Nzwalo

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Irreversible Hypersomnolence after Bilateral Thalamic Infarction

Universidade do Algarve

Irreversible hypersomnolence after bilateral thalamic infarction

Sapientia (Univ. do Algarve)

Letters to the Editor167Journal of Neurosciences in Rural Practice ¦ Volume 9 ¦ Issue 1 ¦ January-March 2018Access this article onlineQuick Response Code:Website: www.ruralneuropractice.comDOI: 10.4103/jnrp.jnrp_465_17This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.How to cite this article: Onder H. Serial diffusion-weighted imaging in transient global amnesia? J Neurosci Rural Pract 2018;9:166-7.© 2018 Journal of Neurosciences in Rural Practice | Published by Wolters Kluwer - MedknowHalil OnderDepartment	of	Neurology,	Yozgat	City	Hospital,	Yozgat,	TurkeyAddress for correspondence: Dr. Halil Onder, Department of Neurology, Yozgat City Hospital, Yozgat 66000, Turkey. E-mail: halilnder@yahoo.comReferences1.	 Sivakumar	 V,	 Indiran	 V.	 Transient	 global	 amnesia.	 J	 Neurosci	Rural	Pract	2017;8:S102.2.	 Sedlaczek	 O,	 Hirsch	 JG,	 Grips	 E,	 Peters	 CN,	 Gass	 A,	Wöhrle	 J,	 et al.	 Detection	 of	 delayed	 focal	MR	 changes	 in	 the	lateral	 hippocampus	 in	 transient	 global	 amnesia.	 Neurology	2004;62:2165‑70.Irreversible Hypersomnolence after Bilateral Thalamic Infarctioninfarction	 [Figure	 1c‑f].	 She	 was	 discharged	 after	 2	weeks	 with	 persistent	 hypersomnolence,	 responding	 to	motor	stimuli	and	falling	asleep	in	the	absence	of	motor	stimulation	 (GCS	 =	 10).	 The	 electroencephalogram	 did	not	 show	 any	 epileptiform	 activity.	After	 3	months,	 she	did	 not	 recover	 and	 kept	 remarkable	 hypersomnolence,	precluding	 regain	 of	 autonomy	 (modified	 Rankin	score	 of	 4).	 The	 combination	 of	 behavior,	 oculomotor,	and	 visual	 abnormalities	 without	 significant	 motor	dysfunction	 is	 suggestive	 of	TBS.[2]	 In	 our	 patient,	TBS	was	caused	by	distal	basilar	 artery	cardioembolic	 stroke	due	 to	 atrial	 fibrillation.	 The	 presence	 of	 simultaneous	occlusion	 of	 proximal	 left	 posterior	 cerebral	 artery,	bilateral	 midbrain	 perforating	 branches	 as	 also	bilateral	 thalamoperforating	 branches,	 caused	 the	 left	occipital,	 the	 bilateral	 midbrain	 infarcts	 and	 the	 BPTS	respectively.	 In	 majority	 of	 cases	 of	 BPTS	 or	 in	 cases	of	 isolated	 midbrain	 lesions,	 progressive	 recovery	 of	consciousness	 occurs.[1‑3]	 However,	 recovery	 in	 our	patient	was	hampered	by	the	presence	of	bilateral	 lesion	of	 the	 paramedian	 thalamic	 nucleus	 which	 is	 involved	in	 consciousness	 regulation	 as	 also	 damage	of	midbrain	structures	 containing	 the	 reticular	 activating	 system.[3,4]	Our	 patient	 presented	 outside	 the	 formal	 time	 window	for	thrombolysis	(≤4.5	h)	and	mechanical	thrombectomy	(≤6	 h).	 However,	 mechanical	 thrombectomy	 can	 be	performed	 with	 good	 results	 up	 until	 24	 h	 of	 basilar	occlusion	 onset.[5]	 Therefore,	 clinical	 suspicious	 of	distal	 basilar	 disease	 should	 be	 considered	 in	 every	patient	 presenting	 the	 combination	 arousal,	 ocular,	visual,	 and	motor	 dysfunction,	 particularly	 in	 the	 era	 of	effective	acute	 reperfusion	 interventions	 for	 large	vessel	occlusions.Sir,Acute	 bilateral	 paramedian	 thalamic	 stroke	 (BPTS)	is	 rare.	 In	 isolation,	 BPTS	 is	 most	 often	 secondary	 to	occlusion	 of	 the	 artery	 of	 Percheron,	 a	 single	 dominant	thalamoperforating	 artery	 arising	 from	 the	 initial	segment	 of	 the	 posterior	 cerebral	 artery	 supplying	 both	paramedian	 thalami.[1]	 However,	 when	 combined	 with	occipital	 posterior	 cerebral	 artery	 infarct,	 the	 “Top	of	 the	 basilar	 syndrome”	 (TBS),	 which	 is	 caused	 by	vascular	 disease	 of	 the	 distal	 basilar	 artery,	 should	 be	considered.[2]	 An	 87‑year‑old	 right‑handed	 female	 with	medical	 history	 of	 hypertension,	 insomnia,	 and	 chronic	back	 pain	 was	 found	 unresponsive	 at	 home.	 She	 was	last	 seen	 in	 her	 normal	 health	 status	 12	 h	 earlier.	 She	was	 admitted	 to	 the	 emergency	department	 (ED)	with	 a	Glasgow	 Coma	 Score	 (GCS)	 of	 9,	 hypotension	 (90/60	mmHg),	 hypothermia	 (36°C),	 and	 bradycardia	 (40	beats/min).	 The	 rest	 of	 the	 neurological	 examination	was	 unremarkable.	 The	 complementary	 metabolic	 and	toxic	 routine	 ED	 investigation	 yielded	 negative	 results.	The	 brain	 computed	 tomography	 showed	 the	 presence	BPTS	 and	 midbrain	 infarction	 [Figure	 1a	 and	 b].	 She	was	 stabilized	 after	 supportive	 treatment	 few	 hours	later.	 During	 hospitalization,	 she	 was	 newly	 diagnosed	with	 hyperlipidemia	 and	 paroxysmal	 atrial	 fibrillation.	The	 rest	 of	 stroke	 workup	 including	 the	 cervicocranial	magnetic	 resonance	 angiography	 yielded	 negative	results.	 Although	 the	 general	 status	 improved	progressively,	 with	 hemodynamic	 stability,	 on	 the	 3rd	day,	 a	 slight	 right‑sided	 hemiparesis	 and	 an	 incomplete	left‑sided	 third	 nerve	 palsy	 were	 noticed.	 The	 brain	magnetic	 resonance	 imaging	 showed	 the	 presence	of	 BPTS,	 midbrain,	 and	 the	 left	 occipital	 lobe	 acute	

Irreversible hypersomnolence after bilateral thalamic infarction

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Universidade do Algarve

Sapientia (Univ. do Algarve)