Age: 67.0
Sex: F
Vaccine: FLU3
Symptoms: Ultrasound scan normal, Ultrasound skull
Clinical narrative: Initial report was received 12 October 2010 from a health care professional. A 67-year-old female patient with no concurrent illness, had received an intramuscular injection of FLUZONE HIGH-DOSE, lot number U3607AA on 30 September 2010, and 11 days (also reported as 10 days) after vaccination, she experienced symptoms of partial amnesia, lapses in memory. The patient was seen in the emergency room and cleared of a diagnosis of a stroke. CT scan was normal. The patient had not received any other vaccines within four weeks of vaccination. The patient had a past history of hypertension, "thyroid", and brain surgery two years ago at which time a facial nerve was wrapped in Teflon. Concomitant medications included Sertraline, Lisinopril, HCTZ and SYNTHROID. It was further reported that the patient experienced these same symptoms previously (date not reported), and per the reporter, it was unclear if the symptoms were related to a previous Influenza vaccine. Outcome was not recovered. Follow-up information received from a health care professional on 16 November 2010 reported that the patient received the FLUZONE HD in the left deltoid. The lapses of memory had duration of approximately five days and she only had short term memory loss. The patient's medical history was updated to include the "thyroid" problem was hypothyroidism and that the patient had an episode of Global Transient Amnesia within 2 weeks after her previous flu vaccine which was given 28 September 2009. The patient's testing included computed tomography scans (CAT scans) and cardiac Doppler. The possibility of stroke, seizures and dementia were ruled out. The patient had a recent loss of her dogs and within 2 weeks after receiving the FLUZONE HD she became confused and was looking for her dead dogs. The neurologist had ruled out the vaccine as the cause and was looking at the traumatic effects of her husband and dogs that triggered her short term memory loss. The patient was now seeking a possible psychological cause for her memory loss. The patient recovered except with some short term memory deficit which still remained. The diagnosis of Global Transient Amnesia was given. The outcome was reported as recovered. Follow-up information was received from a health care professional on 20 December 2010, and included hospital records. The patient had a history of global amnesia in 2009, and was taking aspirin concomitantly. Additional medical history included hypertension, hypothyroidism, depression, and hypercholesterolemia. She also had a history of facial nerve decompression, for which she had undergone craniotomy in April 2009, and facial spasms. Family history was notable for Alzheimer's disease, diabetes, and coronary artery disease. Concomitant medications included hydrochlorothiazide, ZOLOFT, lisinopril, and SYNTHROID. One week prior to admission, the patient had fallen while hiking, but did not report having any concussion. Five days prior to admission, she had tripped and fallen again, with no loss of consciousness. According to a hospital admission note date 11 October 2010, the patient woke up that morning with symptoms of poor memory, i.e. she forgot that her husband was supposed to travel that day and was looking for a dog which had died 2 weeks previously. Her speech was sometimes incoherent and not understandable. She was taken to the emergency department complaining of a headache, where a CAT scan showed calcification in the left cerebellopontine angle region and mild white matter degenerative changes; basic metabolic profile was essentially normal. She was discharged home, and later that day was seen in the neurology clinic where she was noted to have ongoing confusion. Upon examination, she had an increased heart rate of 100, and was alert and oriented to person and place but not year. Short-term recall was decreased, and Mini-Mental status score was 24/30. Cranial nerves were intact with full visual fields, full extraocular pupils, facial expression was symmetric, and tongue was midline. Motor exam showed 5/5 strength in both upper and lower extremities, sensation was intact, and no changes were noted in her gait. An EEG showed excessive slow waves with increased delta and theta activity mixed with faster rhythm, present in both hemispheres. The impression by the neurologist was possible transient global amnesia, however the patient was admitted to the hospital in order to rule out stroke. Transcranial Doppler and carotid Doppler were negative for clots; echocardiogram was also negative. An MRI showed no changed from February 2009 other than "fairly significant maxillary sinus disease" increased in size since the previous exam. She did not exhibit any seizures, numbness, or weakness during her hospitalization, and slowly progressed to almost baseline by the time of her discharge on 13 October 2010. New medications included simvastatin and PLAVIX for stroke prophylaxis. Discharge diagnosis was transient global amnesia. On 01 December 2010, the patient was seen by her neurologist in follow-up. Mental status examination at that time was unremarkable, although she did complain of a loss of smell and taste, which the neurologist noted to be associated with a possible neuro degenerative process. At that time it was noted that the patient had been diagnosed with obstructive sleep apnea 5 years earlier, for which she had not been treated, and the patient continued to experience excessive daytime somnolence. She was scheduled for a polysomnogram study in follow-up. The patient's first event from 28 September 2009 was captured in case 2010-06550. Documents held by sender: none.