Where am I? Interhospital Geriatric Meeting Dr. SL Kwok / Dr. YF Mak Queen Elizabeth Hospital

Transcription

1 Where am I? Interhospital Geriatric Meeting Dr. SL Kwok / Dr. YF Mak Queen Elizabeth Hospital

2 Case 1 Mr. X M/75 referred from GP for sudden onset of confusion and memory loss suspecting of acute stroke

3 background NKDA Retired taxi driver Non smoker social drinker (small amt of beer / wine at occasions) Lives with wife Walks unaided, ADLI 5-6 years of formal schooling

4 Past medical history HT Adalat R 20mg bd dyazide 1 tab daily Eczema on aqueous cream and prn piriton FU GOPD otherwise good past health

5 History of presenting illness Presented with sudden onset confusion and memory loss on the day of admission no Hx of background memory loss Noticed by wife sudden memory loss and abnormal behaviour on the day of admission Did not remember what he did that morning after leaving home for morning exercise Also cannot recall events in the preceding few days on admission

6 Daily routine get up from bed at ~ 06:30 go out for morning exercise at ~ 07: 30 go to restaurant after exercise, usually at ~ 08:30 go to market to buy food for the day buy newspaper and get the letter from the mailbox, and be back to home by ~ 10:30

7 What happened? on the day of admission go out of home for morning exercise as usual but back home later than usual, at noon With the food, letter but not the newspaper patient cannot provide a detail account to wife of why he come late patient did not recall some recent event including his BIL admitted to hospital, his son is going to get marry and he had played mahjong 2 days ago

8 Go to restaurant to meet his friends as usual, appear to be normal and chat with them and comment on recent news appropriately He was also seen by his friend in the market at usual time, appear to be normal

9 History of presenting illness (con t) No witnessed convulsion No other associated symptoms including fever, dizziness, headache, weakness, numbness, slurring of speech or swallowing difficulty No facial asymmetry was noted No intake of other drugs besides the antihypertensives No previous head injury Completely normal the day before

10 History of presenting illness (con t) BIL recently admitted to hospital for illness for ~ 10/7, currently in a critical condition and may succumb used to have good relationship with his sister and brother-in-law and visit them frequently patient is mildly affected by this incidence and appear to be absent-minded lately forgot to turn off tap occasionally after that incidence, but no background memory loss

11 History of presenting illness (con t) Patient was bring to GP clinic for consultation patient keep repeatedly ask why he was taken here and there, what he was doing, what s the time and where he was

12 Physical examination GCS 15/15, oriented Power full over 4 limbs No cerebellar signs CN intact Speak coherently and appropiately No carotid bruit Chest clear /CVS / abd unremarkable

13 Investigations ECG SR no ischemia or arrhythmia CBP normal RLFT normal Random glucose 5.6 TG 1.3 / TC 5.3 / LDL 3.1 TSH normal

14 VDRL : non reactive B12 : 278 Folate : 25.4 urine toxicology : metabolite of piriton only S/B EEG (2/2) : no epileptiform activities MMSE : 29/30

15 CT brain 1/2/10 No focal abnormal brain parenchymal attenuation. No acute hemorrhage. No extra-axial fluid collection. Ventricles are normal in size and shape. No discrete space-occupying lesion seen. repeated CT brain 3/2/10 no serial changes

16 Case 2 Mr. Y Bring by wife to AED after presented with acute onset of confusion and abnormal behaviour

17 Background M/67 Non drinker Hx of high BP, seen herbalist on herbal remedies otherwise good past health

18 What happened? back to home at ~ 2:00pm appear normal initially when he come back home go to turn on the hi-fi and play some music become confused around 1/2 hr later

19 found the home appear untidy to him, with all his CDs and hi-fi component being not in the usual order, but in fact not he go to pour out all his CDs onto the floor asking who make the mess appear to retain his own identity and where he is then the home environment suddenly appear tidy again to him, asking who have just tidied up the place

20 then c/o facial flushing BP taken by wife at that time 178/114 a few repeated measuring showing similar reading patient then rushed to toilet and turned on the water tap with water pouring onto his head, and patient claim he want to 'cool down himself' patient repeatedly asking wife to repeat measure BP for him, claiming that she had not done it yet no prior history of similar episode

21 The next day Patient become normal again can only recall the detail when he initially go back home cannot recall the key event which resulted in this admission however the memory before and after were very clear to him he can even recall which CD he played before the event denied drug or alcohol use

22 Physical examination GCS 15/15 on admission coherent speech and obey command Full power Cranial nerve intact No cerebellar sign abd soft Cardiovascular / chest / abdominal exam unmarkable

23 Investigation CBP normal RLFT normal Fasting glucose 5.3 urine toxicology -ve TG 0.8 / TC 5.5 / LDL 3.8

24 CT brain : No focal abnormal brain parenchymal attenuation. No acute hemorrhage. No extraaxial fluid collection. Ventricles are normal in size and shape. No discrete space-occupying lesion seen S/B EEG : (prelim report) no sharp waves, symmetrical normal background

25 Transient global amnesia

26 Introduction A clinical syndrome of reversible anterograde amnesia Anterograde amnesia : inability to form new memory repetitive questioning occurs in middle-aged and elderly individuals

27 First described in 1956 in 2 case series The term Transient Global Amnesia was introduced and been used since 1964 However, the exact etiology and pathophysiology is still not completely understood up till now

28 Epidemiology incidence General population : 3-8 / 100,000 > 50 years old : / 100,000 majority of episodes occur in individuals between the ages of 50 and 80 mean age of onset : No sex predilection Association with migraine in some case

29 Pathophysiology Primary site of involvement is the mediobasal temporal lobe and hippocampus involved in the formation and retrieval of new episodic memories Supported by neuroimaging DWI-MRI studies in acute and subacute stages of TGA demonstrated lesions in the hippocampus high resolution imaging studies have specifically implicated the CA-1, Sommer sector

30 Pathophysiology (con t) Lesions are most often unilateral and left-sided, but right-sided and bilateral lesions also occur dominant-side hippocampal lesions : prominent verbal memory loss nondominant hippocampal lesions : prominent visuospatial memory deficits

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32 Etiology Remained uncertain No single cause can fully explain the whole clinical picture Probably multiple causes Hypothesis Arterial ischemia Venous congestion Migrainous phenomenon Epileptic phenomenon

33 Arterial ischemia -- pros Had some similar feature with TIA Occur in older adult Usually resolve within 24 hrs Reported in setting with thromboembolic risk vertebral artery angioplasty and stenting basilar artery thrombosis aortic dissection hypercoagulable conditions Hippocampus represent a watershed area between two major arteries DWI-MRI signal abnormality in hippocampus are often described in patients with TGA

34 Arterial ischemia -- cons Difference in some clinical features TGA episodes are longer in duration than typical TIAs TGA patients have a lower atherosclerotic risk burden than patients with TIA patients with TGA have a lower risk of future stroke and death, and resembles that of an age-matched population TGA appears to be precipitated by events that are not associated with TIA (eg. Valsalva maneuver)

35 Arterial ischemia -- cons DWI MRI finding DWI lesion are not specific to only TIA / stroke lesions were no more common in TGA patients than in age- and sex-matched controls lesions seen in TGA are somewhat atypical of those seen in TIA TIA had larger lesions TIA are more likely to be observed in the first few hours of symptoms onset TIA are more likely to evolve into a permanent T2 abnormality

36 Venous congestion -- pros Trigger event Valsalva maneuver vigorous activity of the arms sympathetic activation from acute emotional events cold water immersion increases in either intrathoracic pressure or venous return could lead to central venous congestion affecting the deep venous system that drains the dorsomedial thalamus and hippocampus

37 Venous congestion -- pros Doppler USG studies indicate TGA patients are more common to have jugular valvular insufficiency with demonstrable venous reflux

38 Venous congestion -- cons side of apparent valvular insufficiency did not always correlate with the dominant side of venous blood flow or with the lateralization of DWI lesions Questions unanswered : Why the venous congestion and/or ischemia is selective to the anatomic structures related to memory Why TGA isn't seen more frequently with venous sinus thrombosis Why recurrence is so infrequent if the abnormality can be induced by a Valsalva maneuver Why it only occurs in older adults

39 Migrainous phenomenon Pros Studies demonstrate association with migraine Cons younger age group in migraine Migraine is typically a recurrent disease

40 Clinical features Prominent anterograde amnesia (inability to form new memories) May appear to be disoriented in time or place often repetitively ask questions about the date or their environment Immediate recall (eg, digit-span) is intact delayed recall is impaired Retrograde amnesia is common more variable can extend back hours to days, weeks, and rarely years

41 Other cognitive functions are spared able to perform complex motor tasks during spell such as driving, cooking, lecturing, and playing a musical instrument mean duration of episodes is approximately six hours, most last between 1 and 10 hours

42 When the spell resolves the retrograde amnesia usually completely resolves or is isolated to a brief time immediately preceding the event Patients are left with an amnesic gap for the main episode Associated symptoms headache (10-40%) Nausea, nonspecific dizziness, anxiety, paresthesias

43 Triggering event acute emotional events chronic emotional stress physical events (eg, strenuous activity, sexual intercourse, Valsalva maneuver) postural changes medical procedures high altitude contact with water and/or changes in body temperature Prior episode is unlikely, < 5% Physical exam is usually unremarkable

44 Diagnosis Based on clinical features No confirmatory diagnostic test Exclude possible differential diagnoses

45 Diagnostic criteria

46 Lancet Neurol 2010; 9:

47 Differential diagnoses Seizure TIA / stroke Stroke syndrome presenting with isolated amnesia without other focal neurological symtpoms is associated with lesion in the mesial temporal lobe, caudate nucleus, cingulate gyrus, and splenium of the corpus callosum Delirium Usually a more global confusion and inattention

48 Differential diagnoses Other possible differential diagnoses Head injury anoxic event (carbon monoxide exposure) Hypoglycemia Intoxication drug or alcohol withdrawal herpes simplex encephalitis

49 Proposed diagnostic criteria Information about the beginning of the attack is available from a capable observer. This is to exclude head trauma or loss of consciousness at the onset. Clouding of consciousness or loss of personal identity should be absent. Patient should be examined during the attack to be certain that there are no accompanying neurologic signs or symptoms besides antegrade amnesia The memory loss should resolve within 24 hours. Epileptic features must be absent. Patients with active epilepsy are excluded

50 Investigation No specific diagnostic test available Aim to exclude possible DDx Appropriate initial workup Serum electrolyte Glucose Toxicology screening Brain imaging eg. CT Further evaluation depend on clinical suspicion including EEG, especially recurrent episodes

51 Treatment Not necessary in clear case of TGA Advised to observe patient in hospital until the episode subsided Treatment may be necessary if alternative diagnoses is identified eg. CVA / seizure

52 Prognosis Usually recover without any neurological deficit Recurrent rate is low : annual rate is estimated to be % However, recent studies found that residual memory deficit may occur in patient with TGA high-resolution T2-reversed MRI of the hippocampus showed a significantly higher frequency of cavities in the hippocampus than controls, suggesting permanent neuronal loss in the Sommer or CA1 sector subclinical residual deficits may be common one or more years by neuropsychologic testing