KAWAMATA Miwako

KOMORI Makiko

MUKUBO Yukiko

Tokyo Women’s Medical University

Transient Global Amnesia in a Patient withPostherpetic Neuralgia著者名 MUKUBO Yukiko, KAWAMATA Miwako, KOMORI Makikojournal orpublication titleTokyo Women's Medical University Journalvolume 2page range 37-39year 2018-12-25URL http://hdl.handle.net/10470/00032122doi: 10.24488/twmuj.2017004(https://doi.org/10.24488/twmuj.2017004)37―37―J.TWMU 2: 37-39, 2018Case ReportTransient Global Amnesia in a Patient with Postherpetic NeuralgiaYukiko MUKUBO１,2, Miwako KAWAMATA２, and Makiko KOMORI２１Department of Anesthesiology, Nadogaya Hopspital, Nagoya, Japan２Department of Anesthesiology, Tokyo Women’s Medical University Medical Center East, Tokyo, Japan(Accepted February 13, 2018)(Advance Publication by J-STAGE May 11, 2018)Transient global amnesia (TGA) is a clinical syndrome of reversible anterograde amnesia that occurs in the middle-aged andelderly individuals. The etiology is obscure, and many underlying factors have been reported. We describe an 83-year-oldman with postherpetic neuralgia (PHN) for which he received pregabalin, fentanyl, and a serotonin-norepinephrine reuptakeinhibitor (SNRI). Pain intensity on a numeral rating scale (NRS) was 8/10. He had no history of vascular disease or epilepsy.On November 28th 20XX he visited our hospital and underwent intercostal nerve block with phototherapy as usual. He wasslightly feverish and had a body temperature of 37.8°C with no other symptoms. After 15 minutes rest, he left our hospitaland tried to return to his home, but he was unsure which train to take. About 4 hours later, he suddenly knew where he wasand got back to his home uneventfully. He had been amnetic for several hours. Two weeks later, he was referred to a neurolo-gist, and the episode was diagnosed as TGA. Brain magnetic resonance imaging (MRI) showed non-specific cerebral atrophywith signs of aging at that point. Differential diagnoses include ischemia, migraine, epileptic seizures, and thromboemboliccerebrovascular disease. The cause of TGA remains controversial. However, drugs such as GABAergic drugs, SNRIs, andopioids are known to have effects on cognitive function. Polypharmacy can result in substantial drug-drug interactions, espe-cially in elderly patients. The trigger of this episode in our patient is unclear, but multiple analgesics might have been a causalfactor of his symptoms of TGA.Key Words: global amnesia, postherpetic neuralgia, polypharmacyIntroductionTransient global amnesia (TGA) is a clinical syndromethat was proposed by Hodges and Warlow in 1990１）.TGAis characterized by the sudden onset of anterograde am-nesia lasting up to 24 hours without compromise of otherneurologic functions in middle-aged and elderly indi-viduals. We report a case of TGA associated withpostherpetic neuralgia (PHN).Case PresentationAn 83-year-old man was given a diagnosis of herpeszoster in the Th8-9 region in June 20XX. He was referredto our hospital to receive pain management in August20XX. He complained of continuous and shooting pain(intensity 7 of 10 on a numerical rating scale[NRS]) inhis chest and back, associated with allodynia. He had nohistory of vascular or cerebral diseases, epilepsy, diabetesCorresponding Author: Yukiko Mukubo, Department of Anesthesiology, Tokyo Women’s Medical University Medical Center East, 2-1-10 Nishi-Ogu, Arakawa-ku, Tokyo 116-8567, JapanE-mail: yumukuan@gmail.comdoi: 10.24488/twmuj.2017004CopyrightⒸ 2018 Society of Tokyo Women’s Medical University38―38―Fig.　1　Magnetic resonance imaging (MRI) of the patient.Axial diffusion-weighted imaging (DWI) taken 2 weeks after epi-sode revealed only slight ischemic change.mellitus, myocardial infarction,mental diseases, or recenthead injury. He also had no histry of temporary memoryloss. No other medication was administered by anothermedical department. After thoracic epidural brocks andintercostal nerve brocks were performed 10 times, thepain score decreased to 3 of 10 on the NRS. We gave thepatient pregabalin 300 mg/day, celecoxib 200 mg/day,and vitamine B12 1,500 μg/day.In November, we changed the prescription to amitrip-tyline 20 mg/day and pregabaline 300 mg/day because heclaimed to have compressive pain. In October 20XX＋1he had increasing pain (NRS7/10) associated with the de-creasing atmospheric temperature in the winter season.We replaced amitriptyline with duloxetine 20 mg/day,and decreased the dose of pregabaline to 225 mg/day be-cause he was staggering. On October 20XX＋2, the pa-tient claimed to have increasing pain (NRS7/10) in thewinter season again, and we therefore prescribed anopioid analgesic (fentanyl patch 1 mg/day), pregabaline150 mg/day, and duloxetine 20 mg/day. No side effectdeveloped. In July 20XX＋3, fentanyl patch 2 mg/day,pregabaline 125 mg/day, and duloxetine10 mg/day de-creased the pain intensity to NRS2/10, but he had mildsleepiness. In October the pain increased to NRS8/10again. On November 28th he visited our hospital and re-ceived intercostal nerve block with 0.5 % bupivacaine 5ml with phototherapy as usual. Before the treatment hewas slightly feverish (37.8°C) with no other symptoms.There was no abnormal behavior or conversation beforeor during our examination.On the way back to his home, the patient suddenly for-got how to get home and which train to take. About 4hours later, he suddenly knew where he was, and he wentback to his home in the evening without any injury, palsyor visual or speech disturbances. He had had amnesia forseveral hours. After returning to his home and on the fol-lowing days, his physical and mental status was the sameas usual. However, he did not remember what had hap-pened to him. There was no witness to his behavior dur-ing the amnestic period.After 2 weeks he consulted a neurologist, and the epi-sode was diagnosed as TGA. The mini-mental state ex-amination (MMSE) score was 21/30, indicating slightcognitive impairment. He had never undergone theMMSE before the event. His families mentioned hisslight forgetfulness for several months. However, noother abnormal behavior was reported. Brain magneticresonance imaging ( MRI ) showed non-specific slightcerebral atrophy associated with signs of aging (Fig. 1)Treatment with duloxetine and pregabaline was discon-tinued, and there was no deterioration of amnesia for atleast 8 months after the episode.DiscussionThe diagnosis of TGA is clinical and one of exclusion.Differential diagnoses include several other transient am-nesic disorders with varying epidemiology and diseasecourses２）. Transient epileptic amnesia (TEA) is a rareform of temporal epilepsy, often associated with motorautomatisms of brief duration, occurrence on awakening,and multiple attacks. Prominent and short durations ofretrograde amnesia occur in patients with TEA. Our pa-tient did not have a past history of epilepsy, and antero-grade amnesia began during the daytime, persisted forabout 4 hours, and presented as a single event of disori-entation to place. Transient ischemic attack (TIA) usuallylasts for less than 1 hour with some other symptoms,such as palsy, speech disturbances, or perception distur-bances. Patients with psychogenic amnesia have isolatedretrograde amnesia. Brain MRI with diffusion-weightedimaging (DWI) can demonstrate even minute and tran-39―39―sient hippocampal lesions shortly after events in patientwith TGA. In our patient, DWI was not performed duringand shortly after the episode, but TGA was diagnosed onthe basis of the characteristic episodes. He was slightlyfeverish on morning of the presentation, but his physicalcondition did not exacerbate subsequently. Many eventshave been reported to potentially trigger hippocampalischemia, including emotional or physical changes, theValsalva maneuver, postural changes, medical proce-dures, and changes in body temperature２）. Fever on theday of onset might have triggered our patient’s illness.Pregabarin and duloxetine are popular drugs for the man-agement of PHN. Opioid analgesics are also recom-mended for intractable PHN３）. Because our patient hadrecurrent exacerbations of pain in association with at-mospheric temperature changes in the winter season, weneeded to increase the doses of analgesics, which led topolypharmacy. Drug-drug interactions induced bypolypharmacy are known to cause cognitive disfunction２）.Some analgesic or hypnotic drugs can also affect cog-nitive function. Anticholinergic drugs such as tricyclicantidepressants or benzodiazepines may cause cognitivedisfunction, but serotonin-noradrenaline reuptake inhibi-tors are not considered to worsen it.Opioids and pregabalin have effects on the GABAer-gic receptor system, thereby affecting cognitive func-tion４）. Pickering et al. reported cognitive impairment andpain associated with antidepressants in patients withPHN. Chronic pain itself might also impair cognitivefunction５）.We consider drug-drug interactions the most likelycause of TGA in our patient.ConclusionWe must exercise care and carefully administer drugsthat affect cognitive function when treating elderly pa-tients with chronic pain.Consent for publication was obtained from the patient.Conflicts of Interest: None of the authors of this manu-script have a conflict of interest to declare.References1）Hodges JR, Warlow CP: Syndromes of transient amne-sia : towards a classification. A study of 153 cases. JNeurol Neurosurg Phschiatry 53: 834―843, 19902）Spiegel DR, Mccroskey AL, Deyerle BA: A case of tran-sient global amnesia. Innov Clin Neurosci 13 (3-4): 32―41, 20163）The Committee for the Guidelines for the PharmacologicManagement of Neuropathic Pain of JSPC: Guidelinesfor the Pharmacologic Management of Neuropathic Pain.Shinko Trading, Tokyo (2011)4）Mizukami K: Drug-induced cognitive inpaiment. Psy-chiat Neurol Jap 111: 947―953, 2009 (in Japanese)5）Pickering G, Pereira B, Clère F et al: Cognitive functionin older patients with postherpetic neuralgia. Pain Prac14: E1―E7, 2014

Transient Global Amnesia in a Patient with Postherpetic Neuralgia

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Transient Global Amnesia in a Patient with Postherpetic Neuralgia

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