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Epilepsy & Behavior 9 (2006) 197–203

Case Report

Prosopagnosia following nonconvulsive status epilepticusassociated with a left fusiform gyrus malformation

Helen Wright a, Joanna Wardlaw b, Andrew W. Young c, Adam Zeman d,*

a Department of Clinical Psychology, University of Edinburgh, Edinburgh EH8 9A9, UKb Department of Clinical Neurosciences, Western General Hospital, Edinburgh EH4 2XU, UK

c Department of Psychology, University of York, York YO10 5DD, UKd Peninsula Medical School, Mardon Centre, Exeter EX2 4UD, UK

Received 28 February 2006; revised 8 April 2006; accepted 11 April 2006Available online 14 June 2006

Abstract

A 67-year-old, right-handed woman became unable to recognize familiar faces following a period of nonconvulsive status epilepticus.Neuropsychological assessment revealed a relatively selective impairment of familiar face recognition in the absence of low-level visualdeficits or widespread cognitive impairment. MRI scanning demonstrated an isolated lesion, probably a venous angioma, involving theleft fusiform gyrus, mirror-symmetrical to the site typically linked to prosopagnosia. Potential explanations for the patient’s prosopag-nosia include seizure-related damage to a left fusiform region required for fully competent face recognition and damage to the contra-lateral fusiform gyrus via interhemispheric connections. Focal neuropsychological deficits in patients with refractory partial epilepsy whodevelop nonconvulsive status epilepticus may be underdiagnosed.� 2006 Elsevier Inc. All rights reserved.

Keywords: Prosopagnosia; Face recognition; Epilepsy; Mirror focus; Neuropsychological deficit; Fusiform gyrus

1. Introduction

Focal epileptic activity can give rise to transient postictalsymptoms, ‘‘Todd’s paresis,’’ affecting motor, sensory, andsometimes cognitive capacities. However, permanent focalneuropsychological sequelae from seizures are rare [1]. Thebest-documented examples are of permanent amnesic syn-dromes occurring after prolonged seizures, usually inpatients who have already undergone temporal lobectomy[2]. A recent report describes permanent sensory deficitsand aphasia following prolonged, repeated, status epilepti-cus accompanied by cortical laminar necrosis. We report acase of prosopagnosia following a period of probable non-convulsive status epilepticus. We believe that this case is ofinterest for several reasons: (1) it provides a rare example of

1525-5050/$ - see front matter � 2006 Elsevier Inc. All rights reserved.

doi:10.1016/j.yebeh.2006.04.010

* Corresponding author. Fax: +01392 662929.E-mail address: adam.zeman@pms.ac.uk (A. Zeman).

impaired face recognition associated with structuralpathology in the left fusiform gyrus; (2) it raises the possi-bility that seizure-related neuropsychological deficits canoccur as a result of damage to structures mirror-symmetri-cal to the seizure source; (3) it offers further evidence thathighly focal neuropsychological deficits can result fromprolonged seizure activity.

2. Methods

The patient was referred as an outpatient to one of the authors (A.Z.)in 2000 for continuing neurological care. The following neuropsychologi-cal tests were administered subsequently:

2.1. General cognitive functioning

Cognitive functioning was screened using the Mini-Mental StateExamination (MMSE) [3], which is a brief quantitative measure of cogni-tive status. We then performed a comprehensive cognitive assessmentusing the Wechsler Adult Intelligence Scale III (WAIS-III) [4], which

198 Case Report / Epilepsy & Behavior 9 (2006) 197–203

includes vocabulary, working memory, perceptual organization, and speedof processing subtests and is used to calculate a Full Scale IQ (FSIQ). Inaddition, the National Adult Reading Test (NART) [5] was used to esti-mate overall cognitive ability.

2.2. Verbal memory

The Logical Memory subtests of the Wechsler Memory Scale III(WMS-III) [6] were used to assess verbal memory. These tests require astory to be recalled, immediately and after a delay.

2.3. Visual memory

Visual Memory was assessed using the Rey–Osterrieth Complex FigureTest [7], which requires a design to be recalled after a 30-minute delay.

2.4. Perception and object recognition

The Rey–Osterrieth Complex Figure Test [7] was also used to assessperceptual functioning. This test requires a design to be copied and isscored according to accuracy. The Visual Object Space Perception (VOSP)Test [8] assesses object and space perception, while minimizing the involve-ment of other cognitive skills. The Object Drawings Test [9] was used toassess object recognition. Line drawings of various objects from the Livingand Nonliving categories are presented for recognition.

2.5. Recognition memory: Words and faces

The Recognition Memory Test [10] was used to compare ability to rec-ognize words and faces from previously presented items.

2.6. Facial feature recognition

The Benton Facial Recognition Test (BFRT) [11] was used to assessthe basic visuoperceptive processes involved in face perception. It requiresmatching a sample face to one of several targets.

2.7. Eye gaze sensitivity

The Eye Gaze Sensitivity Test [12] was used to assess the ability tojudge the direction of eye gaze.

2.8. Face and name recognition

In the Face and Name Recognition Task: 1991 Lineups [12], 30 famousfaces are randomly mixed with 10 photographs of nonfamous people. Ayes/no judgment is made as to whether the face is familiar or not. If a faceis familiar, the name or any identifying information is requested. The sec-ond part of the test replaces the photographs with names.

The Famous Faces Test [13] and Graded Faces Test [14] were also usedto assess ability to recognize, name, and provide identifying informationfrom photographs of faces. The Famous Names Test [13] assesses the abil-ities to recognize the names of famous people and to retrieve informationabout them.

2.9. Facial expression recognition

A test using 60 photographs of facial expressions from the Ekman andFriesen series [15] was administered on two occasions to assess ability torecognize facial expressions of basic emotions.

2.10. Famous building recognition

The Famous Buildings Test [12] includes photographs of 20 familiarlandmarks and buildings (such as the Eiffel Tower and Statue of Liberty)and 10 unfamiliar landmarks and buildings. Following recognition of the

familiar buildings and rejection of the unfamiliar buildings, the name ofthe landmark or building is requested. The Graded Buildings Test (AhmedS, Arnold R, Thompson SA, Graham KS, Hodges J. Naming objects, fac-es and buildings in mild cognitive impairment. In preparation) was alsoused to assess the ability to identify and provide information aboutfamous buildings from photographs.

3. Case report

3.1. Clinical history

The patient is a right-handed, 67-year-old woman. Atthe age of 14, she began to have ‘‘trancelike’’ episodes,diagnosed as ‘‘petit mal,’’ approximately twice a month.At age 18, she developed infrequent tonic–clonic seizures.Prior to admission to a psychiatric ward in 1970, at age34, she began to have frequent, almost continuous, epi-sodes of deja vu—‘‘it’s like seeing a film you have seenbefore’’—associated with a sense of prescience and‘‘peculiar bodily feelings, e.g., tingling in the left sideof her face, a feeling of floating in the air looking downon her body and a feeling of compulsion to do things.’’She remained in this state for 2 weeks until she wastransferred to a neurology unit, where an EEG revealeda ‘‘focal right temporal abnormality and generalizedirregular spike and wave discharges.’’ A diagnosis ofnonconvulsive status epilepticus was suggested. Treat-ment resolved the experiential abnormalities, includingthe deja vu, but she complained ‘‘incessantly about diffi-culty with remembering people’s faces.’’ This complaintpersisted thereafter. Despite treatment, she continued tohave tonic–clonic seizures, sometimes preceded by dejavu, witnessed complex partial seizures, and episodes ofdeja vu occurring independently. An EEG in 1977revealed ‘‘intermittent epileptiform phenomena in the leftfrontotemporal region,’’ a CT scan showed a ‘‘deep, pos-terior lesion in the left temporal lobe, just below the tri-gone,’’ which was ‘‘of vascular density and enhanced.’’ Aleft carotid and vertebral angiogram was normal. Shesuffered recurring episodes of depression and often com-plained of poor memory. A third EEG in 1985 revealeda right posterior temporal slow wave abnormality. Nosignificant abnormalities have ever been detected on neu-rological or ophthalmological examination.

The authors first encountered the patient in 2000,when she mentioned her difficulty in recognizing familiarfaces. She said that she found it much easier to recognizepeople from their voices than from their faces. Her rela-tives introduced themselves by name when they came tothe door, and she reported difficulty in recognizing evenextremely familiar faces on television. She was not awareof difficulty in recognizing familiar places, but describedsometimes picking up the wrong object in the kitchen,raising the possibility of a mild object agnosia. Most ofthe neuropsychological testing detailed in Table 1 wasperformed in 2000. We also report some results frommore recent testing.

Table 1Neuropsychological assessment summarya

Results 2000 Results 2004

General cognitive functioning and memory tests

Mini-Mental State Examination (MMSE) 30/30 25/30National Adult Reading Test (NART) ‘‘High average’’ rangeWAIS III Full Scale IQ 94 (‘‘average’’)Wechsler Memory Scale III

Logical Memory (Immediate Condition) 12/25 (+0 SD)Logical Memory (Delayed Condition) 11/25 (+0.7 SD)

Rey–Osterrieth Complex FigureCopy 36/36 (+0.7 SD)Delayed Recall (30 minutes) 12/36 (�1 SD)

Visual Object Space Perception Test (VOSP) ‘‘Passed’’ 8/8 tests ‘‘Passed’’ 8/8 testsObject Drawings Test

Living 16/20: outside range of scores forcontrols aged 50+ (17–20)

Nonliving 16/20: outside range of scores forcontrols aged 50+ (1–20)

Tests of face, name, building perception, and memory

Recognition Memory TestWords 46/50 (+0.7 SD)Faces 21/50 (�4.9 SD)

Benton Facial Recognition Test 44/54 (‘‘normal’’) 46/54 (‘‘normal’’)Eye Gaze Sensitivity Test 16/18 (M = 16.86)Face and Name Recognition Task: 1991 Lineups

Face Lineup: Familiar FacesFamiliarity 19/30 (�3.6 SD)Occupations 9/30 (�6.2 SD)Names 8/30 (�3.9 SD)

Face Lineup: Unfamiliar FacesCorrect Rejections 8/10

Names Lineup: Familiar NamesFamiliarity 27/30: bottom end of normal range (27–30)Occupations 27/30: bottom end of normal range (27–30)

Names Lineup: Unfamiliar NamesCorrect Rejections 10/10

Famous Faces TestRecognized as ‘‘famous’’ 21/60 (�4.9 SD)Named 1/60 (�3.1 SD)Identifying information 13/60 (�2.8 SD)

Famous Names TestRecognized as ‘‘famous’’ 56/60 (+6 SD)Identified information 49/60 (+0 SD)

Graded Faces TestNamed score 8/30 (�4.3 SD)Information score 10/30 (�4.3 SD)

Ekman and Friesen Facial Expression Test 45/60 (overall raw score): ‘‘cutoff’’score in published norms is 41

41/60 (overall raw score): ‘‘cutoff’’ scorein published norms is 41

Famous Buildings TestRecognition of familiar buildings 9/20 (�3.8 SD)Correct rejection of unfamiliar buildings 10/10 (+0.7 SD)Naming of familiar buildings 9/20 (�2.0 SD)

Graded Buildings TestNamed score 8/30 (�4.2 SD)Information score 17/30 (�2.9 SD)

Handedness test

Edinburgh Handedness Inventory 32/32 (right-handed)

a See test references for origins of normative data.

Case Report / Epilepsy & Behavior 9 (2006) 197–203 199

3.2. MRI findings

In 1998, magnetic resonance imaging (MRI) revealed asmall lesion in the left posteromedial temporal cortex lying

adjacent to the tentorium (Figs. 1–4). On the coronal imag-es the lesion lay in the collateral sulcus and involved themedial fusiform gyrus and, posteriorly, the lateral parahip-pocampal gyrus [16]. The fusiform cortex was thinned, par-

lesion

hippocampus

Sylvian fissureLateral ventricles

Collateral sulcus

Lateral occipito-temporal sulcus

Inferior temporal gyrus

Fusiform gyrus

Fig. 1. T1 MRI coronal image of the brain, showing enhancing lesionmedial to the left fusiform gyrus, which is reduced to a small triangle oftissue.

Fig. 2. Line drawing indicating the positions of structures labelled inFig. 1.

Lateral ventricles Sylvian fissure

hippocampus

Inferior temporal gyrus

Lateral occipito-temporal sulcus

lesion

Collateral sulcus

Fusiform gyrus

Fig. 3. T1 MRI coronal image of the brain posterior to the image shownin Figs. 1 and 2. The fusiform gyrus arches round and is thinned by thelesion.

Fig. 4. Line drawing indicating the positions of structures labelled inFig. 3.

200 Case Report / Epilepsy & Behavior 9 (2006) 197–203

ticularly anteriorly, where it was reduced to a small triangleof tissue (Figs. 1 and 2). Posteriorly, the medial cortex ofthe fusiform gyrus arched around and was thinned by thelesion (Figs. 3 and 4). The lesion was also close to, andindented posteriorly, the lateral border of the parahippo-campal gyrus. There was serpiginous enhancement withinthe lesion and a small flow void. The appearance was con-sistent with a benign vascular lesion such as venous angio-ma. There were no other focal abnormalities. In particular,the right medial and inferior temporal lobe structuresappeared normal.

3.3. Neuropsychological assessment

A detailed neuropsychological assessment of currentcognitive functioning and face recognition ability wascompleted in 2000, and followed up with further investiga-tions in 2004. The results are summarized in Table 1.

The neuropsychological assessment revealed averageintelligence with concordant general memory functioning.Her performance on the VOSP Test was normal, but shewas just below the range of normal control scores on theObject Drawings Test, indicating minor generalized difficul-ty with visual recognition. Her normal performance on theBenton Facial Recognition Test and Eye Gaze SensitivityTest excludes a generalized deficit in face perception. Hervery poor performance on the tests of novel and famous facerecognition (Face and Name Recognition Task and FamousFaces Test) indicates a selective deficit of face memory. Hernormal performance on famous name recognition tests(Face and Name Recognition Task and Famous NamesTest) confirm that her difficulty in recognizing famous facesis not due to a generalized loss of semantic information aboutfamous people, but rather to a problem in accessing thisknowledge via face perception. Her impairment on the

EXPRESSION ANALYSIS

FACIAL SPEECH ANALYSIS

DIRECTED VISUAL PROCESSING

FACE RECOGNITION UNITS

PERSON IDENTITY NODES

NAME GENERATION

View-centred descriptions

Expression-independent descriptions

STRUCTURALENCODING

Or

COGNITIVE SYSTEM

Fig. 5. Bruce and Young’s [17] functional model of face recognition.

Case Report / Epilepsy & Behavior 9 (2006) 197–203 201

famous building tests, (Famous Buildings Test and GradedBuildings Test) again suggests that her difficulty in recogniz-ing famous faces may not be specific to faces. The results ofthe Ekman and Friesen Facial Expression Test were withinthe normal range.

4. Discussion

The patient developed symptoms of prosopagnosia fol-lowing a period of EEG-confirmed nonconvulsive statusepilepticus. MRI scanning demonstrated a vascular anom-aly in the left fusiform gyrus. This is likely the underlyingcause of her epilepsy. Prosopagnosia is as a rule associatedwith bilateral or right-sided fusiform pathology. We pro-pose that the patient’s prosopagnosia is the result of bilat-eral fusiform gyrus dysfunction, resulting from the episodeof prolonged nonconvulsive status epilepticus. We discussthe background and implications of this hypothesis next.

4.1. Prosopagnosia due to a left-sided structural lesion

The term prosopagnosia describes an inability to recog-nize faces that cannot be attributed to low-level visuoper-ceptual or global cognitive impairments. The patient’sdifficulties in recognizing familiar faces are clearly of the‘‘prosopagnosic’’ type: She could recognize most familiarpeople from their names, and did not suffer generalizedvisual or intellectual problems; however, her face recogni-tion deficits were moderately severe, rather than the near-absolute loss noted in many of the published cases.

Prosopagnosia is usually the result of a traumatic or vas-cular insult, a degenerative process, or a cerebral tumor.Functional models have been developed to account forthe multiple cognitive components involved in face process-ing and the selective patterns of impairment observed.Bruce and Young proposed the most influential of thesemodels in 1986 [17] (Fig. 5). The model proposes that thereare separate pathways for the processing of facialexpressions, the directed visual analysis required to matchunfamiliar faces, facial speech, and the recognition offamiliar faces.

Recent research on face perception using functionalimaging underlines the distinction between the analysesof invariant and of changeable aspects of the face [18].Using functional brain imaging evidence, Haxby et al.[18] demonstrated that the invariant aspects are mediatedby the face responsive region in the fusiform gyrus, andthe changeable aspects, by the face responsive region inthe superior temporal sulcus. These findings are consistentwith the Bruce and Young model [17].

The location of the minimum lesion required for proso-pagnosia is still controversial. Prosopagnosia is most oftendescribed in association with bilateral or occasionally unilat-eral right occipitotemporal lobe pathology [18,20]. Mattsonet al. [19] reported a case of prosopagnosia following lefthemisphere injury in a left-handed individual, but very rea-sonably suggest that this may be explained by an atypical

pattern of hemispheric specialization of function. In the con-text of prosopagnosia due to unilateral right temporal lobepathology [21,22], De Renzi et al. have suggested that thereis variation in the degree of hemispheric specialization forface recognition within the population [21]. The occurrenceof face recognition impairment in association with a leftoccipitotemporal lesion in a right-handed patient, as in thiscase, could be explained in terms of De Renzi and colleagues’hypothesis, on the assumption that the capacity for face rec-ognition was equally distributed between the two hemi-spheres in the patient. Alternatively, the occurrence ofdisturbed face recognition following a period of probablenonconvulsive status epilepticus in our patient could haveled to the creation of a ‘‘mirror lesion.’’

4.2. A ‘‘mirror lesion’’?

The occurrence of apparently independent EEG spikesin a homotopic area contralateral to a spiking epilepto-genic lesion was first observed in human surgical casesin 1946 by Pope et al. [23] and became referred to asa ‘‘mirror focus.’’ Morrell demonstrated experimentallythat following the creation of an epileptic primary focus,an independent epileptic focus can develop in the homo-topic area of the contralateral hemisphere, that is, theregion to which the primary focus sends a direct synapticprojection [24–26]. Rigorous exploration of primary epi-leptic sites has indicated that mirror foci develop indirect proportion to the number of commissural fibers[27]. For example, mirror foci rarely develop from aprimary lesion in the primate motor cortex, as thisregion is almost devoid of callosal connections.

202 Case Report / Epilepsy & Behavior 9 (2006) 197–203

The patient’s primary lesion (and probable primaryfocus) is in the left fusiform gyrus. The details of theinterhemispheric connections between regions of the fusi-form gyrus involved in face perception are unclear (Dae-Shik Kim, dskim@bu.edu, e-mail communication to A.Zeman, 8 September 2005).

The literature on mirror foci has focused on their causesand their consequences for postoperative outcome inpatients undergoing epilepsy surgery. Our case suggeststhat prolonged seizure activity may interfere with thefunctioning of the corresponding area of the contralateralhemisphere, with consequences for face recognition.

4.3. Focal neuropsychological deficits following seizureactivity

The patient’s face recognition deficit developed follow-ing prolonged focal seizure activity. Other reports of per-manent seizure-induced focal neuropsychological deficitsare surprisingly rare. Dietl et al. describe two cases ofamnesia and hippocampal atrophy following recurrentepileptic seizures in patients with previous unilateral tem-poral lobectomies, and cite a similar case by Oxburyet al. [2]. In the first of Dietl and colleagues’ two cases,the amnesic syndrome occurred in the wake of noncon-vulsive status epilepticus. Donaire et al. recently reportedtwo cases of permanent neurological and cognitive defi-cits following prolonged, recurrent nonconvulsive statusepilepticus [29]. Though rarely described, such conse-quences are in keeping with accumulating evidence thatboth repeated brief seizures and status epilepticus cancause neuronal death and remodeling of neural networkswith cognitive and behavioral repercussions [30]. We can-not exclude the possibility that some other pathologicalevent, for example, ischemia or hemorrhage in the leftfusiform gyrus, gave rise both to the patient’s episodeof nonconvulsive status epilepticus and to her prosopag-nosia. However, there is no direct evidence to supportthis suggestion.

There is growing recognition of transient remote effectsof seizures, such as reversible cerebellar diaschisis [31].Transient cognitive deficits following focal seizures, includ-ing dysphasia and amnesia, are also relatively common[32,33]. It is possible that subtle, permanent, focal cognitivedeficits, such as the patient’s face recognition problems,may be an underrecognized complication of repeated orprolonged focal seizures.

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