Anterograde amnesia, brain fornix, ischaemic stroke, postoperative period

A stroke following total joint arthroplasty is rare, occurring in around 0.2% of patients [1]. The first 2 weeks after arthroplasty are high risk in terms of developing an ischemic stroke, with almost a five times greater risk compared to that in an age-adjusted population. The risk remains high for about 6 weeks, with the greatest risk occurring in the immediate postoperative period [2]. Cerebral hypoperfusion, marrow embolization, and anesthetic effects on the cardiovascular system have been cited as possible mechanisms underlying this ischemic risk [1,2].
Ischemic strokes affecting the anterior fornix are also an infrequent occurrence, with just a few case reports published [3-8]. All these case reports demonstrated a link between acute amnesia and fornix infarcts. The role of the anterior fornix in memory function is related to its anatomical placement within the Papez circuit, which comprises the fornix, hippocampus, mammillary bodies, anterior thalamus, and cingulate gyrus [9,10]. The anterior fornix acts as the output tract from the hippocampus, primarily to the mammillary bodies. The primary function of the Papez circuit, which was first described in 1937, involves encoding and recall of new, episodic information. Memory function is more reliant on the structural integrity of the circuit as a whole rather than the integrity of each of the individual components [9,10].
In this paper, a case of a patient who developed a post - operative fornix infarct and anterograde amnesia is described, followed by a discussion of the relationship between the anterior fornix and memory function and the role of hypoperfusion brain injury in ischemic strokes.

The case of a patient who developed postoperative anterograde amnesia due to a fornix infarct was described. This case reveals the relationship between the anterior fornix and memory function, as well as the role of hypoperfusion brain injury in ischemic strokes. Acute fornix infarcts are rare, and previous case reports describe acute amnesia as the main presenting symptom [3-8]. Two of these cases were due to an isolated fornix infarction [3,4], while the other cases [5-8], including the one described herein, were associated with ischemia of nearby structures, including the corpus callosum and cingulate gyrus. Interestingly, the case of the isolated left anterior fornix injury [4] was not clinically different to the case with the isolated bilateral fornix infarction [6], suggesting that isolated fornix lesions can cause amnesia and a lack of laterality to fornix function. This may be due to the dual role of the fornix as a tract from the thalamus to the basal forebrain and as a commissure between the left and right hemispheres [9].
Multiple pathologies can damage the anterior fornix, either on their own or as part of a diffuse process. These include congenital absences, neoplastic diseases, infections, autoimmune diseases, metabolic diseases, infarctions, and traumas. Isolated fornix infarcts almost exclusively occur in the anterior columns. This is likely due to the proximity of the remaining fornix to the choroidal arterial supply aiding collateral perfusion and protecting against infarctions [9]. Blood to the anterior fornix is supplied by branches of the anterior communicating artery (ACoA) [9], which accounts for the high rate of postoperative amnesia in ACoA aneurysm surgery [11,12]. Other variations to the vascular supply that can cause anterior fornix infarctions include occlusion of the subcallosal artery [8] or the anterior cerebral artery via short medial central arteries [3]. Approximately 20–50% of poststroke patients have subjective complaints of memory difficulties, which may be accounted for by nonanatomical etiologies, such as depression, fatigue, medication side-effects, or sleep disorders. However, lesions within memory-associated structures or amnesic lesions and lesions impairing memory processing (process lesions) should be considered [10]. Pathological processes affecting hippocampal and diencephalic connections are consistently more likely to impair memory function than fornix lesions [10,13]. Interestingly, in a case study on 142 epileptic patients who underwent bilateral anterior fornix transection, no patients experienced long-term memory impairment [14].
In the present case, the fornix infarct occurred during the perioperative period. Hypoperfusion of the fornix during the period of hypotension contributed to the infarct in this case. The combination of systemic hypotension and preexisting extracranial arterial occlusive disease caused a reduced blood supply, which led to a hemodynamic stroke [15]. In this patient, carotid Doppler ultrasound revealed 50–69% stenosis in the right internal carotids. Although this level of stenosis is considered only mild-to-moderate, the concurrent hypotension likely contributed to the hypoperfusion and the hemodynamic stroke. Hypotension is a known cause of ischemic strokes, with a high risk among those with symptomatic orthostatic hypotension and cardiac failure [15]. Intraoperative blood pressure has been shown to be directly related to the neurological outcome following cardiac surgery, with almost 50% of patients undergoing cardiac surgery having MRI evidence of bilateral ischemic lesions in “border zone” areas between the main brain vascular supplies, which are vulnerable areas to ischemic injury. [16] The risk of watershed infarcts was higher in patients with an intraoperative fall in systolic blood pressure of 10 mmHg or more [16]. Another study found radiological evidence of strokes in 7.2% of patients with intraoperative mean arterial pressure of 50–60 mmHg as compared to 2.4% when mean arterial pressure was maintained between 80 and 100 mmHg [17]. Thus, maintaining blood pressure and brain perfusion during the intraoperative and postoperative periods is important to reduce the risk of ischemic strokes.
In the present case, the patient required an intensive multidisciplinary assessment and treatment at an inpatient specialized acute brain injury rehabilitation service. The patient was discharged after 3 months of inpatient rehabilitation. Early initiation of postacute rehabilitation treatment in brain injury is beneficial and increases the likelihood of a functional improvement [18]. The mechanism underlying such recovery is likely multimodal, ranging from controllable factors (motivation, family support systems, and rehabilitation service quality) to uncontrollable factors (age, sex, injury severity and site, and premorbid cognitive reserve) [19].
The long-term cognitive outcome after acute fornix infarcts is uncertain. One study described a patient who developed amnesia and confabulation following astrocytoma removal, which disrupted the right anterior fornix. [13] This patient made a good recovery over a 17-month follow-up period, suggesting that recovery is possible in the long term. Compensatory measures by the left anterior fornix likely account for recovery in such patients [13]. However, a remaining functional fornix is not a prerequisite for memory recovery, as observed in patients who improved cognitively after bilateral fornix transection [20].

Authors’ contributions

The author contributed solely to the article.

Conflict of interest

The author declared that there are no conflicts of interest.

Consent for Publication

Written informed consent for publication of de-identified case details and radiological images were obtained from the patient (witnessed by the son).

1. Mortazavi S M J, Kakli H, Bican O, et al. Perioperative stroke after total joint arthroplasty: prevalence, predictors, and outcome. JBJS, 2010, 92(11): 2095-2101.

2. Lalmohamed A, Vestergaard P, Cooper C, et al. Timing of stroke in patients undergoing total hip replacement and matched controls: a nationwide cohort study. Stroke, 2012, 43(12): 3225-3229.

3. Moudgil S S, Azzouz M, Al-Azzaz A, et al. Amnesia due to fornix infarction. Stroke, 2000, 31(6): 1418-1419.

4. Korematsu K, Hori T, Morioka M, et al. Memory impairment due to a small unilateral infarction of the fornix. Clinical neurology and neurosurgery, 2010, 112(2): 164-166.

5. Renou P, Ducreux D, Batouche F, et al. Pure and acute Korsakoff syndrome due to a bilateral anterior fornix infarction: a diffusion tensor tractography study. Archives of neurology, 2008, 65(9): 1252-1253.

6. Rizek P, Pasternak S, Leung A, et al. Acute-onset anterograde amnesia caused by isolated bilateral fornix infarction. Canadian journal of neurological sciences, 2013, 40(5): 738-739.

7. Saito Y, Matsumura K, Shimizu T. Anterograde amnesia associated with infarction of the anterior fornix and genu of the corpus callosum. Journal of Stroke and Cerebrovascular Diseases, 2006, 15(4): 176-177.

8. Moussouttas M, Giacino J, Papamitsakis N I H. Amnestic syndrome of the subcallosal artery: a novel infarct syndrome. Cerebrovascular Diseases, 2005, 19(6): 410.

9. Lim C, Alexander M P. Stroke and episodic memory disorders. Neuropsychologia, 2009, 47(14): 3045-3058.

10. Thomas A G, Koumellis P, Dineen R A. The fornix in health and disease: an imaging review. Radiographics, 2011, 31(4): 1107-1121.

11. Gade A. Amnesia after operations on aneurysms of the anterior communicating artery. Surgical neurology, 1982, 18(1): 46-49.

12. Hattingen E, Rathert J, Raabe A, et al. Diffusion tensor tracking of fornix infarction. Journal of Neurology, Neurosurgery & Psychiatry, 2007, 78(6): 655-656

13. Ruggeri M, Sabatini U. Recovery from amnesic confabulatory syndrome after right fornix lesion. Neurorehabilitation and neural repair, 2008, 22(4): 404-409.

14. Garcia-Bengochea F, Friedman W A. Persistent memory loss following section of the anterior fornix in humans. A historical review. Surgical neurology, 1987, 27(4): 361- 364.

15. Klijn C J M, Kappelle L J. Haemodynamic stroke: clinical features, prognosis, and management. The Lancet Neurology, 2010, 9(10): 1008-1017.

16. Gottesman R F, Sherman P M, Grega M A, et al. Watershed strokes after cardiac surgery: diagnosis, etiology, and outcome. Stroke, 2006, 37(9): 2306-2311.

17. Gold J P, Charlson M E, Williams-Russo P, et al. Improvement of outcomes after coronary artery bypass: a randomized trial comparing intraoperative high versus low mean arterial pressure. The Journal of thoracic and cardiovascular surgery, 1995, 110(5): 1302-1314.

18. Hayden M E, Plenger P, Bison K, et al. Treatment effect versus pretreatment recovery in persons with traumatic brain injury: a study regarding the effectiveness of postacute rehabilitation. PM&R, 2013, 5(4): 319-327.

19. Wilson B A. Brain injury: recovery and rehabilitation. Wiley Interdisciplinary Reviews: Cognitive Science, 2010, 1(1): 108-118.

20. Mazarakis N K, Summers F, Murray A D, et al. Partial recovery from amnesia following bilateral surgical fornix transection is correlated with cortical plasticity. British journal of neurosurgery, 2011, 25(5): 658-661.