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Year : 2022  |  Volume : 9  |  Issue : 2  |  Page : 69-71

Aphasia as the initial manifestation of herpes encephalitis

1 Department of Pediatrics, The Indus Hospital, Karachi, Pakistan
2 Department of PICU, The Indus Hospital, Karachi, Pakistan

Date of Submission01-Sep-2020
Date of Decision25-Nov-2020
Date of Acceptance21-Dec-2020
Date of Web Publication30-Mar-2022

Correspondence Address:
Dr. Muhammad Shahzad
The Indus Hospital, Karachi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JPCC.JPCC_141_20

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Pediatric acquired aphasia is an uncommon presenting complaint in children. Because of many etiologies that may prove fatal, it is essential to take immediate essential steps for diagnoses and treatment. We are presenting a 9-year-old child who was conscious, alert and did not have any other systemic findings at presentation. After initial and then more extensive workup, he was diagnosed with herpes encephalitis. Acyclovir has been started as empirical antiviral therapy. In the course of disease, he developed status epilepticus that was controlled with multi anti-epileptic drugs. Intravenous acyclovir continued for 21 days, and anti-epilepticus medicines were given at discharge.

Keywords: Aphasia, children, clinical features, encephalitis, etiologies, outcome, stroke

How to cite this article:
Shahzad M, Ghafoor A, Jurair H. Aphasia as the initial manifestation of herpes encephalitis. J Pediatr Crit Care 2022;9:69-71

How to cite this URL:
Shahzad M, Ghafoor A, Jurair H. Aphasia as the initial manifestation of herpes encephalitis. J Pediatr Crit Care [serial online] 2022 [cited 2023 Feb 3];9:69-71. Available from: http://www.jpcc.org.in/text.asp?2022/9/2/69/341443

  Introduction Top

Pediatric acquired aphasia (PAA) is a rare, multifactorial, broadly categorized problem faced in children after a healthy development phase.[1] Known etiologies are related to cranial trauma, cerebral tumors, encephalitis, ischemic, and hemorrhagic strokes.[2] In some cases, Aphasia has also been described as a presenting feature of hypomagnesemia.[3] Nonfluent aphasia (Broca's Aphasia) is an uncommon presentation of encephalitis.[4] Encephalitis may be secondary to autoimmune problems or infection. Viruses such as herpes simplex virus (HSV), enterovirus, influenza, and varicella Zoster (VZ) are mentioned as common etiologies in children.[5] HSV may lead to herpes simplex encephalitis (HSE), as also reported in developing countries (10.5%). A broad spectrum of clinical manifestations ranges from mild fever and headache to complete coma in such cases.[6],[7] We are describing a case here that presented in our hospital with fever and unable to speak.

  Case Report Top

A 9-year-old child, weight 21 kg and height 118 cm, was presented in emergency with a fever complaint for 2 days, headache, and unable to speak for 1 day. However, he was cooperating but was unable to speak the words. His mother noticed that he was unable to hold anything with the right hand and walk-in line. He has a low-grade fever, no chills, and rigors, continuous and relieves with antipyretic therapy. He complained of headaches, mild intensity, diffuse, intermittent, not disturbing his sleep pattern, and no specific time and place. There was no history of vomiting, ear discharge, difficulty swallowing, vision loss, rash, seizures and decease consciousness, staring gaze, or irrelevant movements. He was a regular school-going child with good progress. There was no past hospitalization, his vaccination was up to date without any event, and he has unremarkable birth and development history.

On examination, his vitals were heart rate 116, respiratory rate 28, and temperature 38.6, bp 100/60. On central nervous system examination, his Glasgow Coma Scale (GCS) was 15/15 with proper orientation but unable to speak, the normal tone in all limbs, power 4/5 on the right side of the body. Deep-tendon reflexes were 2+ in all limbs, and superficial reflexes were intact. Plantar reflexes were static. His signs of meningeal irritation were absent. Cranial and cerebellar signs were intact. Other systemic examinations were standard.

He was suspected of having cerebral insult secondary to an infection, stroke, electrolyte imbalance, or an autoimmune problem based on history and examination. His Random blood sugar (RBS) was 112 mg/dl; other electrolytes, including Sodium, Potassium, Calcium, and Magnesium level, were in the normal range. Anti-neutrophilic antibody was also normal. Maintained intravenous (IV)-line, IV ceftriaxone, and oral paracetamol were prescribed for fever. Computed tomography brain showed mild effacement of sulci and gyri without any gross pathology [Figure 1]. Cerebrospinal fluid (CSF) D/R showed sugar, 67 mg/dl; protein, 18; white blood cell, 31; neutrophils, 1%; lymphocytes, 98%; monocytes, 1%; gram stain, gene expert and CSF culture were negative. This report was in favor of viral etiology. IV acyclovir was started empirically. His CSF was run for HSV by polymerase chain reaction (PCR) that came positive after 1 week of admission. At the 8th day of admission, he developed two episodes of seizures 1 h apart that started as focal then became generalized. Seizures were controlled with midazolam and levetiracetam. His GCS start deteriorating, and he was shifted to the pediatric intensive care unit. He was electively intubated and ventilated. The child developed the status epilepticus that was controlled with levetiracetam, phenytoin, and midazolam. Levetiracetam was started at 15 mg/kg/dose Q6H, and Phenytoin was loaded first with 20 mg/kg and then continued with 2.5 mg/kg/dose Q12H. Midazolam was given intermittently. However, his seizures did not stop. Hence, we added IV lacosamide and topiramate, but seizures continued to occur. Then, he was kept on midazolam infusion for seizures control and other four antiepileptic drugs (AEDS) named levetiracetam, phenytoin, oral topiramate, and IV lacosamide, adjusted in a clockwise fashion, were also given. His seizure status was monitored with Continuous portable electroencephalography (EEG), which showed the right-sided spike waves involving the temporoparietal region [Figure 2].
Figure 1: Computed tomography scan brain plain and with intravenous contrast, showing normal size ventricles, with mild effacement of sulci and gyri

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Figure 2: Electroencephalography showing right sided spike waves involving temporoparietal region

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We planned magnetic resonance imaging (MRI) brain for investigating the complications of encephalitis, such as infarction, demyelination, and bleeding. His brain MRI showed hyperintensities, appreciated in the bilateral frontoparietal and temporal region. On T2 and flair images, MRI showed patchy diffusion restrictions with accumulated meningeal enhancement and cerebral sulci effacement [Figure 3]a and [Figure 3]b. After 5 days, we started tapering his AEDS. We did monitor his phenytoin level, liver function test, and electrolytes twice weekly. Tracheostomy was done to make easy handling of prolonged intubation. He was extubated after 3 weeks of ventilation without any ventilator-associated complications. IV acyclovir was given for 21 days. After 3 weeks of total illness, he recovered his full consciousness. Afterward, he remained stable and discharged home with two AEDS and tracheostomy care.
Figure 3: Magnetic resonance imaging brain T1 image showing hyperintensities, in bilateral fronto-parietal and temporal region (a) On T2, there are diffusion restrictions with accumulated meningeal enhancement (arrow head) and effacement of cerebral sulci (b)

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  Discussion Top

PAA is an unusual presenting complaint secondary to trauma, stroke, cancer therapy, anoxic encephalopathy, and rarely with herpes encephalitis and cat-scratch disease.[8],[9] Although encephalitis is not an uncommon problem being encountered in the pediatric population. With time, its incidence has been raised as also variance in clinical manifestation. Worldwide data report an annual incidence of acute encephalitis ranging from 3.5 to 7.4/100,000, rising to 16/100,000 in children.[4] In a study by Elbers et al., the most common presenting complaint was fever, focal seizures, and hemiparesis, while aphasia was present in only 2 cases.[9] Mortality has resulted in 70% in studies if not diagnosed and treated on time.[10] A clinical clue may add in diagnosis in some cases like a rash, but it may be absent. PCR in CSF is a gold standard test available in many countries for the rapid detection of HSV. Serology is also being performed in many developing countries where the facility of PCR is not available.[6] In addition to determining the causative agent, it is also essential to get CSF d/r, MRI with and without contrast, and EEG.[11] Acyclovir is a currently available drug that has reduced mortality from 70% to 19%.[12] Despite treatment, neurological sequels have been reported in 63% of cases, including seizures in 44% and developmental delay in 25%.[4]

Aphasia, as the initial manifestation of HSE, is an unusual but recognizable feature. Keeping it in the early list of differentials would lead to prompt diagnosis and early management.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.


The author especially thank Dr. Sadiq Mirza, Dr. Abdul Rahim Ahmed for guidance in this entire process.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Hout AV. Acquired Aphasia in Children. ACQUIRED APHASIA IN CHILDREN.7.  Back to cited text no. 1
Loonen MC, van Dongen HR. Acquired childhood aphasia. Outcome 1 year after onset. Arch Neurol 1990;47:1324-8.  Back to cited text no. 2
Dharnidharka VR, Carney PR. Isolated idiopathic hypomagnesemia presenting as aphasia and seizures. Pediatr Neurol 2005;33:61-5.  Back to cited text no. 3
Elbers JM, Bitnun A, Richardson SE, Ford-Jones EL, Tellier R, Wald RM, et al. A 12-year prospective study of childhood herpes simplex encephalitis: Is there a broader spectrum of disease? Pediatrics 2007;119:e399-407.  Back to cited text no. 4
Thompson C, Kneen R, Riordan A, Kelly D, Pollard AJ. Encephalitis in children. Arch Dis Child 2012;97:150-61.  Back to cited text no. 5
Beig FK, Malik A, Rizvi M, Acharya D, Khare S. Etiology and clinico-epidemiological profile of acute viral encephalitis in children of Western Uttar Pradesh, India. Int J Infect Dis 2010;14:e141-6.  Back to cited text no. 6
Fernandes AF, Lange MC, Novak FT, Zavala JA, Zamproni LN, Germiniani FM, et al. Extra-temporal involvement in herpes simplex encephalitis. J Clin Neurosci 2010;17:1221-3.  Back to cited text no. 7
Dennis M. Language disorders in children with central nervous system injury. J Clin Exp Neuropsychol 2010;32:417-32.  Back to cited text no. 8
Fox JW, Studley JK, Cohen DM. Recurrent expressive aphasia as a presentation of cat-scratch encephalopathy. Pediatrics 2007;119:e760-3.  Back to cited text no. 9
Lewis P, Glaser CA. Encephalitis. Pediatr Rev 2005;26:353-63.  Back to cited text no. 10
Messacar K, Fischer M, Dominguez SR, Tyler KL, Abzug MJ. Encephalitis in US children. Infect Dis Clin North Am 2018;32:145-62.  Back to cited text no. 11
Whitley RJ, Alford CA, Hirsch MS, Schooley RT, Luby JP, Aoki FY, et al. Vidarabine versus acyclovir therapy in herpes simplex encephalitis. N Engl J Med 1986;314:144-9.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3]


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