Πρόκειται για την περίπτωση ενός άνδρα 74 ετών, που παρουσίασε διαταραχές συμπεριφοράς μετά από κρανιοεγκεφαλική κάκωση προ 45ετίας. Διαγνώστηκε με μανία και δεν έκανε απεικονιστική εξέταση του εγκεφάλου έκτοτε. Κατά τη νοσηλεία στην κλινική μας, οι CT και MRI εγκεφάλου ανέδειξαν ευμεγέθη γλοιωτική εστία στην περιοχή του δεξιού μετωπιαίου λοβού.We present a case of a 74 years old man, who developed behavioral abnormalities following a brain injury, 45 years ago. He was misdiagnosed with mania and had never had a brain imaging. During hospitalization in our department, brain CT and MRI showed sizable gliosis in the right frontal lobe.t

Antoniadi, Eleni

Kaprinis, Stergios

Kouskouras, Constantinos

Moschopoulos, Nikolaos

Nimatoudis, Ioannis

Tegos, Thomas

English

Aristotle University of Thessaloniki: Open Journals / ΑΡΙΣΤΟΤΕΛΕΙΟ ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΟΝΙΚΗΣ

InTRoduCTIonBehavioral abnormalities, ranging from mildly inap-propriate social behavior to full blown mania, mayresult from frontal lobe lesions. Apart from “frontallobe syndrome,” various names have been used, in-cluding “pseudopsychopathic syndrome1,” “secondarymania2,” “acquired sociopathy3,” “disinhibition syn-drome4.” The fact that patients with brain lesions may developbehavioral and personality changes has been knownfor over 150 years. Perhaps the most famous case isthat of Phineas Gage5, a railroad worker who had abizzare work accident in 1848, damaging his frontallobes. After an explosion, his skull was penetrated byan iron rod. He survived and was able to talk and evenwalk after the accident, but his behavior and personalitychanged dramatically. Specifically, he lost his sense ofresponsibility and became capricious, offensive, disre-spectful, resulting to his dismissal from the job. CASe RepoRTMr N, 74 years old, presented to the psychogeriatricoutpatient clinic, accompanied by his wife, who com-plained about aggression, psychomotor agitation, de-creased need for sleep, elevated and irritable mood,impulsivity, disorganized and sexually inappropriatebehavior, low functioning. These symptoms had grad-ually appeared over the past 45 years, but had deteri-orated significantly during the last two years. The di-agnosis of bipolar disorder (recurrent manic episodes)had been offered to him and he had been hospitalizedin public and private psychiatric departments manytimes, showing only minimal improvement. To the bestof his wife’s knowledge, he had no prior medical history.He was admitted to the 3rd department of psychiatry,in order to examine possible general medical conditionetiology, and to modify his medication.According to him, the psychiatric symptoms hadgradually appeared about 45 years ago, following trau-matic brain injury. He believed that he inherited his“madness” from the village lunatic, when the latter hithim in the head with a heavy stick. He had lost con-sciousness after the brain injury and was admitted toa surgical department. He recovered fully and was dis-charged shortly afterwards. At that time, neither brainCT nor MRI were available. He was able to return toCASe RepoRT*Corresponding author: Nikolaos Moschopoulos, Anaximandrou 75, 54250 Thessaloniki, Greece, tel. no.: (+30)6948604365,e-mail: moshopoulosn@gmail.comFrontal lobe syndrome caused by traumatic brain injury presenting as maniaNikolaos Moschopoulos1, Stergios Kaprinis1, Thomas Tegos2, Eleni Antoniadi2, Constantinos Kouskouras3, Ioannis Nimatoudis113rd Department of Psychiatry, AHEPA Hospital, Aristotle University of Thessaloniki21st Department of Neurology, AHEPA Hospital, Aristotle University of Thessaloniki3Radiology Department, AHEPA Hospital, Aristotle University of ThessalonikiABSTRACT: We present a case of a 74 years old man, who developed behavioral abnormalities following a brain injury, 45years ago. He was misdiagnosed with mania and had never had a brain imaging. During hospitalization in our department,brain CT and MRI showed sizable gliosis in the right frontal lobe.t.Keywords: frontal lobe syndrome, traumatic brain injury, maniahis job as a shepherd, but his behavior and personalitychanged. Prior to his accident, he was a shy and lone-some person. Shortly after the injury, he became moreextrovert. He used to spend much money, drinkingwith friends and gambling. He often engaged in violentconflicts, even when he wasn’t drunk. His symptoms deteriorateded progressively overthe years. Five years after the injury, he was unable towork and became so irritable and physically aggressive,that his relatives requested an order of protective cus-tody. He was hospitalized in a public mental hospital,diagnosed with mania and begun treatment with an-tipsychotics. Mr N’s relatives placed the beginning ofhis mental disorder at the time of his admission to themental hospital, therefore dismissing the brain injuryas a possible cause. Since then he was hospitalized inprivate and public psychiatric departments multipletimes, but had never had a brain CT or MRI beforeadmission to our department. He was also treated asan outpatient, not complying sufficiently with medica-tion. His psychological, social and occupational func-tioning was low, as he was unable to keep a job, ne-glected his family, had few friends, engaged frequentlyin violent conflicts. During the last two years he seemedto develop severe memory problems, which led to afurther disorganisation of his behavior. For instance,he turned on a faucet in the house basement and forgotto turn it off, resulting in the flooding of the entirebasement. His loss of inhibition and self control alsodeteriorated. His wife became alarmed and turned toour psychogeriatric outpatient clinic.On admission, Mr N was alert, oriented and hadgood eye contact. He demonstrated psychomotor ag-itation, impulsivity, disorganized and inappropriatebehavior. For example, he frequently interrupted theclinical interview and sang loudly, entered rooms offemale patients without asking, was constantly joking,especially about sexual matters. His speech was pres-sured, distracted, and occasionally derailed. Neitherdelusions, nor hallucinations were present. His moodwas elevated and irritable. He was only partially coop-erative and demonstrated poor insight and judgement.Neurologically, fine movements, speed and strengthof movements were decreased in the left hand. In ad-dition, deviation of the eyes to the left was incomplete. Prior to admission, he had been treated by a privatepsychiatrist with exceptionally high doses of risperidone(36mg daily), amisulpride (800mg daily), chlorpro-mazine (600mg daily), oxcarbazepine (1200mg daily)and also biperiden (4mg daily), but his symptoms didn’timprove considerably. On admission, the ECG showeda notable QTc prolongation and, consequently, themedication doses were lowered (risperidone 12mgdaily, oxcarbazepine 600mg daily, discontinuation ofchlorpromazine and amisulpride). During the followingdays, the ECG became normal but he demonstratedhypertension (about 180/100mm Hg), that was treatedwith amlodipine 10mg daily. Probably he had a historyof hypertension, which remained undiagnosed due tothe antipsychotics’ hypotension side effect.His laboratory results, including complete bloodcount, basic metabolic, liver and thyroid profile, pro-lactin, vitamin B12 and folic acid, were normal, exceptfrom hyperprolactinemia (950 μIU/ml). A CT scan ofthe brain showed sizable gliosis in the frontal operculumand the precentral area of the right frontal lobe. A fol-lowing brain MRI scan (Fig. 1) confirmed the cerebralCT findings, which could be attributed with a consid-erable degree of certainty to old traumatic brain injury.The Addenbrooke’s Cognitive Examination (ACE-R)revealed severe cognitive decline. Specifically, the gen-eral scores were 20/30 in MMSE and 38/100 in ACE-R and the subscores were 14/18 in attention and ori-entation, 7/26 in memory, 3/14 in fluency, 9/26 in lan-guage and 5/16 in visuospatial abilities. Different drug combinations were tried, in orderto achieve maximum efficacy. Oral risperidone wascontinued (6mg daily) and long-acting risperidone in-jection 50mg was added, due to his history of treatmentincompliance. Quetiapine up to 300mg daily was added,which was replaced later with zuclopenthixol 75mgdaily. Memantine 10mg daily was also added. He grad-ually became less agitated, irritable and impulsive, sleptnormally and was more cooperative. He was dischargedfollowing 25 days of inpatient care, accompanied byhis wife.  dISCuSSIonRegarding Mr N’s case, we ought to highlight the im-portance of laboratory tests and brain imaging to thediagnosis of mental disorders. His behavioral distur-bances had been attributed to bipolar disorder for over40 years and he had never had brain imaging. Ηis rel-atives had considered the brain injury as irrelevant,probably because he needed psychiatric treatment al-most five years subsequent to the incident. Nevertheless,a detailed clinical interview revealed behavioral andpersonality changes right after the brain injury. Fur-26 Aristotle University Medical Journal, Vol. 43, Issue 1, February 2016thermore, his symptoms seemed to deteriorate pro-gressively through the years, whereas exceptionallyhigh doses of antipsychotics, which caused notable sideeffects (hypotension, QTc prolongation), didn’t improvehis symptoms significantly. We questioned the bipolar disorder diagnosis andexamined general medical condition etiology. BrainCT and MRI scans revealed a sizable gliosis in thefrontal operculum and the precentral area of the rightfrontal lobe. Due to the size of the lesion, there can beassumed that nearby areas, such as right orbitofrontalcortex and inferior frontal cortex, were also affected.Numerous studies have shown a significant associationbetween behavioral abnormalities and right frontallobe lesions. Some of them are presented below, thougha comprehensive review of the literature is beyond thescope of this short paper.Starkstein et al (1997)4 described a mechanism ofmotor, sensory, affective, intellectual, and instinctivedisinhibition, resulting from lesions to specific brainareas, especially orbitofrontal and basotemporal cortex.Aron et al (2004, 2014)6,7 proposed that right inferiorfrontal cortex in humans is critical for inhibiting re-sponse tendencies and can be characterized as a“brake,” whose disruption could underpin responsecontrol disorders. James et al (2015)8 examined the ar-chitecture of behavioral disturbances following braininjury. They concluded that physical aggressiveness,verbal aggressiveness and sexually inappropriate be-havior reflect distinct but related clinical phenomena.In a large follow-up study of 113,906 patients, Orlovskaet al (2014)9 investigated the relationship between headinjury and subsequent psychiatric disorders. Head injurywas associated with a higher risk of schizophrenia, de-pression, bipolar disorder and organic mental disorders. Our patient also developed progressively severecognitive decline that led to the further disorganizationof his behavior. Cipolotti et al (2015)10 studied theeffect of age on cognitive performance of frontal pa-tients. The results showed that the combined effect ofaging and frontal lesions impairs the frontal corticalsystems by causing its computational power to fall belowthe threshold needed to complete executive tasks suc-cessfully.Frontal lobe syndrome caused by traumatic brain injury presenting as mania 27Fig. 1 (a) T1 weighted MRI, axial view, shows sizable gliosis involving the frontal operculum and the precentral area of theright frontal lobe. (b) T2 weighted MRI, coronal view. ReFeRenCeS1. Blumer D, Benson DF. Personality changes with frontaland temporal lobe lesions. In Benson DF, Blumer D,eds. Psychiatric aspects of neurologic disease. NewYork: Grune & Stratton, 1975.2. Krauthammer C, Klerman GL. Secondary mania: manicsyndromes associated with antecedent physical illnessor drugs. Arch Gen Psychiatry 1978;35:1333-9.3. Saver JL, Damasio AR. Preserved access and processingof social knowledge in a patient with acquired sociopa-thy due to ventromedial frontal damage. Neuropsy-chologia 1991;29(12):1241-9.4. Starkstein S, Robinson RG.  Mechanism of Disinhibi-tion After Brain Lesions. J Nerv Ment Dis1997;185(2):108-14.5. Damasio H, Grabowski T, Frank R, Galaburda AM,Damasio AR. The return of Phineas Gage: clues aboutthe brain from the skull of a famous patient. Science1994;264:1102-4.6. Aron AR, Robbins TW, Poldrack RA. Inhibition andthe right inferior frontal cortex. Trends Cogn Sci2004;8:170-7.7. Aron AR, Robbins TW, Poldrack RA. Inhibition andthe right inferior frontal cortex: one decade on. TrendsCogn Sci 2014;18:177-85.8. James AI, Böhnke JR, Young AW, Lewis GJ. Mod-elling verbal aggression, physical aggression and inap-propriate sexual behaviour after acquired brain injury.Proc Biol Sci 2015 Jul 22;282(1811).9. Orlovska S, Pedersen MS, Benros ME, Mortensen PB,Agerbo E, Nordentoft M. Head injury as risk factor forpsychiatric disorders: a nationwide register-based fol-low-up study of 113,906 persons with head injury. Am JPsychiatry 2014;171(4):463-9.10. Cipolotti L, Healy C, Chan E, MacPherson SE, WhiteM, Woollett K, Turner M, Robinson G, Spanò B, Boz-zali M, Shallice T. The effect of age on cognitive per-formance of frontal patients. Neuropsychologia2015;75:233-41.Σύνδρομο μετωπιαίου λοβού από κρανιοεγκεφαλική κάκωσημε κλινική εικόνα μανίαςΝικόλαος Μοσχόπουλος1, Στέργιος Καπρίνης1, Θωμάς Τέγος2, Ελένη Αντωνιάδη2,Κωνσταντίνος Κούσκουρας3, Ιωάννης Νηματούδης11Γ′ Ψυχιατρική Κλινική, Νοσοκομείο ΑΧΕΠΑ, Α.Π.Θ.2Α′ Νευρολογική Κλινική, Νοσοκομείο ΑΧΕΠΑ, Α.Π.Θ.3Ακτινολογικό Εργαστήριο, Νοσοκομείο ΑΧΕΠΑ, Α.Π.Θ.ΠΕΡΙΛΗΨΗ: Πρόκειται για την περίπτωση ενός άνδρα 74 ετών, που παρουσίασε διαταραχές συμπεριφοράς μετά απόκρανιοεγκεφαλική κάκωση προ 45ετίας. Διαγνώστηκε με μανία και δεν έκανε απεικονιστική εξέταση του εγκεφάλουέκτοτε. Κατά τη νοσηλεία στην κλινική μας, οι CT και MRI εγκεφάλου ανέδειξαν ευμεγέθη γλοιωτική εστία στην περιοχήτου δεξιού μετωπιαίου λοβού.Λέξεις-Κλειδιά: Σύνδρομο μετωπιαίου λοβού, κρανιοεγκεφαλική κάκωση, μανία.28 Aristotle University Medical Journal, Vol. 43, Issue 1, February 2016

Frontal lobe syndrome caused by traumatic brain injury presenting as mania

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Frontal lobe syndrome caused by traumatic brain injury presenting as mania

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Aristotle University of Thessaloniki: Open Journals / ΑΡΙΣΤΟΤΕΛΕΙΟ ΠΑΝΕΠΙΣΤΗΜΙΟ ΘΕΣΣΑΛΟΝΙΚΗΣ