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Central Neurogenic Hyperventilation Related to Post-Hypoxic Thalamic Lesion in a Child

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Central Neurogenic Hyperventilation Related to Post-Hypoxic Thalamic Lesion in a Child Neurology International 2016; volume 8:6428 Central neurogenic normal. An emergency brain magnetic reso- nance imaging (MRI) was performed. Correspondence: Pinar Gençpinar, Department of hyperventilation related Although there was no apparent lesion in the Pediatric Neurology, Tepecik Training and to post-hypoxic thalamic lesion brain stem, bilateral diffuse thalamic, putami- Research Hospital, Izmir, Turkey. in a child nal and globus palllideal lesions were detected Tel.: +90.505.887.9258. on MRI (Figures 1 and 2). Examination E-mail: [email protected] Pinar Gençpinar,1 Kamil Karaali,2 revealed tachypnea (respiratory rate, 42/min), but other findings were normal. Arterial blood Key words: Central neurogenic hyperventilation; enay Haspolat,3 O uz Dursun4 thalamus; tachypnea; children. Ş ğ gases (ABGs) were pH, 7.52; PaCO2, 29 mmHg; 1Department of Pediatric Neurology, and PaO2, 142 mmHg. The chest radiograph, Contributions: PG prepared the manuscript; KK Tepecik Training of Research Hospital, electrocardiogram, and echocardiogram were prepared the figures and edited in this respect; 2 Izmir; Department of Radiology, normal. Laboratory studies disclosed the fol- OD and SH edited this manuscript and made final 3Department of Pediatric Neurology, lowing values: hematocrit, 33.7%, white blood version. 4Department of Pediatric Intensive Care cell count, 10.6×109/L; sodium, 140 mEq/L; Unit, Akdeniz University Hospital, potassium, 3.7 mEq/L; serum urea nitrogen; 6 Conflict of interest: the authors declare no poten- Antalya, Turkey mg/dL; creatinine, 0.21 mg/ dL; and glucose, tial conflict of interest. 110 mg/dL. Liver transaminases levels were normal. Serum lactate level was 1.97 mmol/L Received for publication: 23 January 2016. (normal range 0.5-2.2). His electroencephalo- Revision received: 1 February 2016. Accepted for publication: 2 February 2016. Abstract gram was normal. His tachypnea could not be treated with analgesia (fentanyl infusion) and This work is licensed under a Creative Commons sedation (midazolam infusion). On the 16th Central neurogenic hyperventilation (CNH) Attribution NonCommercial 4.0 License (CC BY- day of admission hyperventilation resolved NC 4.0). is a rare clinical condition, whose mechanism spontaneously. Tracheostomy was performed is still unclear. Here, we report a 3-year-old and he was discharged from the intensive care ©Copyright P. Gençpinar et al., 2016 male patient, who had bilateral thalamic, puta- unit in vegetative state with normal ventila- Licenseeonly PAGEPress, Italy minal and globus pallideal infarction resulted tion. Neurology International 2016; 8:6428 in CNH without brainstem involvement. This doi:10.4081/ni.2016.6428 case may illustrate a possible role for the thal- amus in regulating ventilation. use Discussion to the brainstem. Based on these informa- tion’s, we thought that thalamic lesion may be Introduction The pathophysiologic mechanism of CNH is more likely causing to CNH in our patient. unclear. It has been shown that in animal mod- To date 44 cases were reported with CNH in els, stimulation of the lateral parabrachial the literature (Supplementary Table S1). Central neurogenic hyperventilation (CNH) nucleus increased the respiratory rate.4,5 Detailed clinical information of five cases was is a rare condition and defined as a syndrome Stimulation of respiratory control areas in the not available. Thirty of 39 patients (77%) had comprising normal or elevated arterial oxygen pons and medulla could explain CNH but it is malignancies such as lymphoma, astrocytoma, tension, decreased arterial carbon dioxide ten- not sufficient. It has been known that pontine glioblastoma and medulloblastoma. Other sion, and respiratory alkalosis with hyperventi- respiratory group neurons modulate the respi- three underlying pathologies of CNH were lation even during sleep.1-3 The diagnosis of ratory rhythm. But animal models that discon- CNH requires the exclusion of pulmonary, car- multiple sclerosis, encephalitis and Anti N- nectcommercial the pontine respiratory group from the metil-D-aspartat encephalitis. Similar to our diac, and metabolic disorders that can result in medulla have not resulted in CNH.6,7 Elevated hyperventilation. To date, 44 cases have been case one patient, who was 79 years old, had CNS lactate levels could be a reason of hyper- CNH due to thalamic infarction without brain- reported in the literature and majority of these ventilation by stimulation of medullary stem involvement.14 Kramer et al. described a cases were secondary to tumoral lesions chemoreceptors.8-11 The lactate levels of our male awake patient, who had chronic lympho- involving the brainstem. We report hereNon a 3- case were in normal range during hyperventi- cytic inflammation with pontine perivascular year-old male patient presented with asphyxia lation state. Theoretically, hyperventilation enhancement responsive to steroids syndrome and diagnosed as CNH related to diffuse thala- could be seen in ictal-period during convul- (CLIPPERS) and diagnosed CNH.15 Majority of mic infarction. sions. Nevertheless intermittent hyperventila- cases (77%) were adult. To our knowledge our tion would be more likely explanation in these case is the youngest patient diagnosed with cases.12,13 No ictal or interictal discharges were determined on electroencephalogram of CNH in the published literature. Case Report our case during hyperventilation. The thala- mus has multiple functions in the brain. The A 3-year-old boy, who was intubated, was thalamus plays a major role in regulating admitted to the emergency care unit. His par- arousal, the level of awareness, and activity. It Conclusions ents had found him unconscious and cyanotic also plays an important role in regulating in the garden and there was a mark of his rain- states of consciousness. Similar to our case, In this report, a 3-year-old male patient, hood on his neck, which suggested suffoca- Johnston et al. described chronic dyspnea and whom had bilateral diffuse thalamic lesion due tion. He was resuscitated twice before his hyperventilation in a patient with subcortical to post-hypoxic damage resulted in CNH, was admission to our hospital. On admission his infarcts in the medial thalamus bilaterally.14 presented. Findings of this case support the Glasgow coma score (GCS) was 3. These cases suggested a possible role for the possible role of thalamus in respiratory con- Electrocardiogram and chest radiograph were thalamus in regulating ventilation in addition trol. [page 12] [Neurology International 2016; 8:6428] Case Report 1994;14:6500-10. 5. Takayama K, Miura M. Respiratory responses to microinjection of excitatory amino acid agonists in ventrolateral regions of the lateral parabrachial nucleus in the cat. Brain Res 1993;604:217-23. 6. Plum F. Mechanisms of central hyperventi- lation. Ann Neurol 1982;11:636-7. 7. Bianchi AL, Denavit-Saubie M, Champagnat J. Central control of breath- ing in mammals: neuronal circuitry, mem- brane properties, and neurotransmitters. Physiol Rev 1995;75:1-45. 8. Nattie E. CO2, brainstem chemoreceptors Figure 1. T2-weighted and diffusion weighted images. Increased intensity on both globus pallidus is present on T2-weighted image. Restricted diffusion is prominent on both thal- and breathing. Prog Neurobiol ami, putamina and globus pallidus. 1999;59:299-331. 9. Severson CA, Wang W, Pieribone VA, et al. Midbrain serotonergic neurons are central pH chemoreceptors. Nat Neurosci 2003;6:1139-40. 10. Richerson GB. Serotonergic neurons as carbon dioxide sensors that maintain pH homeostasis. Nat Rev Neurosci 2004;5: 449-61. 11.only Krendel DA, Pilch JF, Stahl RL. Central hyperventilation in primary CNS lym- phoma: evidence implicating CSF lactic acid. Neurology 1991;41:1156-7. 12. Suzuki M, Kawakatasu T, Kamoshita S, et use al. A case of pontine tumor associated with repeated episodes of hyperventilation and Figure 2. T2-weighted and diffusion weighted images show no pathologic intensity on ketosis. Paediatr Univ Tokyo 1964;10:58- pons. 62. 13. Gottlieb D, Michowitz SD, Steiner I, Wald Neurol 2005;62:1632-4. U. Central neurogenic hyperventilation in 3. Pauzner R, Mouallem M, Sadeh M, et al. a patient with medulloblastoma. Eur References High incidence of primary cerebral lym- Neurol 1987;27:51-4. phoma in tumor-induced central neuro- 14. Johnston SC, Slingh V, Ralston HJ, Gold WM. 1. Plum F, Swanson AG. Central neurogenic genic hyperventilation. Arch Neurol Chronic dyspnea and hyperventilation in an hyperventilation in man. Arch Neurol 1989;46:510-2. awake patient with small sub- cortical Psychiatry 1959;81:535-49. commercial4. Chamberlin NL, Saper CB. Topographic infarcts. Neurology 2001;57:2131-3. 2. Tarulli AW, Lim C, Bui JD, et al. Central organization of respiratory responses to 15. Kramer CL, Wijdicks EF. Central neuro- neurogenic hyperventilation. A case report glutamate microstimulation of the genic hyperventilation. Neurology 2014;83: and discussion of pathophysiology. Arch parabrachial nucleus in the rat. J Neurosci 376. Non [Neurology International 2016; 8:6428] [page 13].
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