Expressive Aphasia As the Manifestation of Hyper
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LETTER TO THE EDITOR Korean J Intern Med 2016;31:1187-1190 https://doi.org/10.3904/kjim.2014.379 Expressive aphasia as the manifestation of hyper- glycemic crisis in type 2 diabetes Ji Hyun Lee1, Ye An Kim1, Joon Ho Moon1, Se Hee Min1, Young Shin Song1, and Sung Hee Choi1,2 1Department of Internal Medicine, To the Editor, height and weight were 167 cm and 63 Seoul National University College Hyperosmolar hyperglycemic state kg, respectively. However, after recur- of Medicine, Seoul; 2Department of Internal Medicine, Seoul National (HHS) is a life-threatening complica- rent nausea and vomiting for several University Bundang Hospital, tion of diabetes mellitus, and it is rela- weeks, the patient had lost 10 kg of body Seongnam, Korea tively common in elderly patients with weight. At the time of his first visit to type 2 diabetes. A variety of neurologi- a hospital in China, his blood glucose cal deficits may occur in patients with level was more than 400 mg/dL (22.2 HHS, including changes in mental sta- mmol/L). tus such as drowsiness, lethargy, deliri- The patient presented at Emergency um, or coma. Seizures, sensory deficits, Department of Seoul National Univer- and visual disturbances also sometimes sity Bundang Hospital upon his return occur in patients with HHS. However, to Korea, exhibiting difficulty finding aphasia, as a neurological deficit, is not the correct words to express himself, commonly associated with hypergly- frequent pauses in speech production, cemia. We report the case of man who and normal comprehension of spoken presented with symptoms of motor language. However, he mistook written aphasia including inability to speak flu- Chinese characters for Korean phonetic ently, concurrent with marked hyper- symbols. Additionally, the patient ex- glycemia. perienced intermittent headache with A middle-aged man presented with a sensation of squeezing that lasted for motor-dominant aphasia lasting for 2 to 3 hours each day. Headaches were 5 days, as well as a history of headache located in the left temporal area. for the past month. He had type 2 di- The patient was dehydrated, but abetes that was previously well-con- alert and oriented at the time of phys- trolled with antidiabetic medications, ical examination. Verbal fluency and Received : December 11, 2014 and he also had hypertension, diabetic repetition were impaired, but compre- Revised : June 10, 2015 retinopathy, and stage 4 chronic kidney hension of spoken language, reading, Accepted : June 14, 2015 disease. There was no history of strokes, writing, and naming skills were intact. Correspondence to seizures, or trauma. The patient relo- Other focal neurologic signs such as Sung Hee Choi, M.D. cated to China for work as an engineer motor weakness, sensory abnormalities, Department of Internal Medi- cine, Seoul National University 2 months prior to hospital admission or involuntary movements were absent. Bundang Hospital, 82 Gumi-ro and had recently experienced a com- The patient’s blood pressure was 173beon-gil, Bundang-gu, mon cold. He had been missing meals 170/99 mmHg and body temperature Seongnam 13620, Korea and not taking his antidiabetic medica- was normal. Laboratory data indicat- Tel: +82-31-787-7033 Fax: +82-31-787-4052 tions since arriving in China because he ed a blood glucose level of 471 mg/dL E-mail: [email protected] disliked Chinese food, except fruit. His (26.2 mmol/L) and serum osmolality of Copyright © 2016 The Korean Association of Internal Medicine pISSN 1226-3303 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/ eISSN 2005-6648 by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. http://www.kjim.org The Korean Journal of Internal Medicine Vol. 31, No. 6, November 2016 A B Figure 1. Axial diffusion weighted image (A), magnetic reso- nance angiography (B) of patient showed no suspicious lesion of acute stroke and arterial stenosis. 312 mOsmol/L. Glycated hemoglobin was 15.8% (149.2 mmol/mol), and venous blood gases indicated a serum pH of 7.388. Serum ketone was 1+, and urine ketone was Figure 2. Electroencephalogram showed slow background 1+. Other electrolyte abnormalities included sodium 128 activity and intermittent irregular delta slow activities in the whole hemisphere. Diffuse cerebral dysfunction was sus- mEq/L, potassium 4.1 mEq/L, chloride 93 mEq/L, bicar- pected which could be seen on metabolic encephalopathy. No bonate 26.8 mEq/L, and urea 42 mEq/L. Serum creatinine evidence of epileptiform discharge was observed. was 2.94 mg/dL. Brain magnetic resonance imaging (MRI), including diffusion-weighted images and magnetic resonance an- to a baseline level. Aphasia did not re-occur during the giography, was performed in order to exclude structural 18-month follow-up period. lesions such as acute stroke or malignancy (Fig. 1). Elec- A wide range of neurological abnormalities occur troencephalogram (EEG) demonstrated slow background with HHS, including lethargy, confusion, delirium, or activity and intermittent irregular delta slow activities in coma. Hemiparesis and chorea have also been observed the whole hemisphere. Diffuse cerebral dysfunction was in patients with HHS, and localized sensory or motor suspected, and the patient experienced metabolic en- weakness may occur. In the present case, motor symp- cephalopathy. No evidence of epileptiform discharge was toms presented as diabetic striatopathy, which is a rare observed (Fig. 2). involuntary movement disorder that occurs when serum Intensive intravenous insulin therapy was administered osmolality reaches 320 to 330 mOsmol/L, and which may at an initial dose of 0.15 U/kg/hr, which was decreased to recover after normalization of fluid deficits. The hypoth- 0.1 U/kg/hr until the blood glucose level had fallen to 250 esized mechanism for chorea in HHS is depletion of mg/dL. Massive fluid replacement was performed using gamma-aminobutyric acid via an anaerobic pathway [1]. isotonic saline to relieve dehydration. Verbal fluency was Aphasia sometimes occurs in cerebrovascular, epi- slightly impaired at this point in treatment, but it gradu- leptic, neurodegenerative, or traumatic conditions. The ally recovered and repetition abilities normalized after 2 most common cause of aphasia is cerebrovascular dis- days in the hospital. The headaches also improved after ease, and aphasia is reported in 20% to 40% of patients glycemic control was achieved. The patient’s blood glu- with stroke [2]. Additionally, seizures may occur in ap- cose level was between 110 and 250 mg/dL after 6 days in proximately 25% of patients with HHS [2]. Table 1 pres- the hospital. He could speak fluently after his hypergly- ents several case reports of aphasic status epilepticus cemia was treated and was discharged from the hospital with hyperglycemia. after 11 days. Electrolyte imbalances improved when the Aphasia is classified by the location of the brain lesion patient was discharged, and serum creatinine decreased and the resulting symptoms. Broca’s aphasia is charac- 1188 www.kjim.org https://doi.org/10.3904/kjim.2014.379 Lee JH, et al. Diabetes presenting as aphasia Table 1. Baseline characteristics, imaging and EEG finding of aphasic status epilepticus patients in previous case reports Aphasia at Age, Glucose, Osmolality, HbA1c, No. Sex Symptom Imaging EEG Management discharge, yr mg/dL mmol/L % day 1 60 F 455 - - Impaired fluency, No focal lesion on Initial EEG epileptiform activity Insulin, No (3) naming and brain CT initiated in the posterior left temporal CBZ 1,200 mg repetition region, with recruiting activity, irradiating to the left frontal region 2 78 M 381 297 13.5 Impaired fluency, Mild cortical Left frontotemporal theta to delta Insulin, No (5) naming, repetition atrophy but no focal waves with epileptiform discharges CBZ 100 mg and comprehension lesion on brain MRI 3 60 F 641 319 8.7 Impaired fluency, No focal lesion on Ictal rhythmic discharges initiated Insulin, No (2) naming and brain CT from left frontal lobe 3 months later: CBZ 400 mg repetition normalized 4 74 M 697 303 16 Impaired fluency, No focal lesion on Seizure discharge over the left Insulin, No (35) naming and brain CT hemisphere phenytoin comprehension EEG, electroencephalogram; HbA1c, hemoglobin A1c; CT, computed tomography; CBZ, carbamazepine; MRI, magnetic resonance imaging. perglycemia producesaglobaldecreaseincerebralper area.Hy frontalcorticesandBroca’s lesions intheleft is similartotranscorticalmotoraphasiaresultingfrom manifestation This strating decreasedrepetitionability. includingdemon speakwell, hecouldnot but intact comprehensionwas thecaseof auditory In ourpatient, [3]. brain areassurroundingthemiddlecerebralartery andthecommonsitesofimpaired, damageareinthe bothrepetitionandcomprehensionareseverely aphasia, globaltemporal gyrusof hemisphere[3].In thedominant sults fromalesionintheposteriorareaof thesuperior re aphasiausually Wernicke’s understanding language. havedeficits in donot they but fluently, ingless words aphasiaspeakmean Wernicke’s with aphasia [3].Patients expressive with associated is hemisphere, dominant in the gyrus frontal inferior the including of brain, the anteriorregion The comprehension. well-preserved ly withrelative but lossofterized by tospeak, theability not prescribe any anti-epileptic medications, whichisin medications, anti-epileptic prescribeany not We did and therewerenoresidualneurological